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1.
Fumex, Maud.
Etude de la sulfatation des protéines dans les processus d’interactions biologiques : cas du récepteur aux chimiokines CXCR4 : Role of protein sulfation in biomolecular interactions : focus on the chemokine receptor CXCR4.
Degree: Docteur es, Sciences de la vie et de la santé, 2018, Université Paris-Saclay (ComUE)
URL: http://www.theses.fr/2018SACLE033
► La sulfatation protéique est une modification post-traductionnelle qui intervient principalement sur les récepteurs cellulaires. Parmi eux, le récepteur CXCR4 est particulièrement étudié en raison de…
(more)
▼ La sulfatation protéique est une modification post-traductionnelle qui intervient principalement sur les récepteurs cellulaires. Parmi eux, le récepteur CXCR4 est particulièrement étudié en raison de son implication dans de nombreux processus physiopathologiques (réponse immunitaire, infection au VIH). Le domaine extracellulaire de 38 acides aminés de CXCR4 (le peptide P38), contenant trois tyrosines connues pour être sulfatées, est important pour l’interaction avec son ligand spécifique, la chimiokine SDF-1α/CXCL12 (Stromal Cell-Derived Factor-1α). Le rôle de la sulfatation de CXCR4 dans cette interaction est encore méconnu.Le peptide P38 a été synthétisé et sulfaté de façon régiosélective sur toutes les tyrosines (peptides mono-, di- ou tri-sulfatés, soit 7 combinaisons). L’impact du nombre et de la position des groupements sulfate le long du peptide P38 sur son interaction avec SDF-1α a été étudié par électrophorèse capillaire d’affinité (ACE) couplée ou non à la spectrométrie de masse électrospray (ESI-MS). Une interaction entre P38 et SDF-1α a été mise en évidence par ACE. Une augmentation de l’affinité peut être associée à l’augmentation du degré de sulfatation de P38. La stœchiométrie des complexes a ensuite été déterminée en utilisant l’ACE-MS, qui a mis en évidence une majorité de complexes 1:1, quel que soit le peptide étudiéCes travaux ouvrent la voie à l'étude d'une interaction à trois partenaires avec des glycosaminoglycanes.
Sulfation is one of the most important post-translational modifications of proteins. The known sulfated proteins are mostly cell receptors and among them, CXCR4 attracts growing attention because of its involvement in numerous physio-pathological processes (immune response, HIV infection). The 38 amino-acid extracellular domain of CXCR4 (P38 peptide), containing three tyrosine residues known to be sulfated, is important for the interaction with its specific ligand, the SDF-1α/CXCL12 chemokine (Stromal cell-derived factor-1α). The role of sulfation in this interaction remains to be established.The P38 peptide was chemically synthesized and regioselectively sulfated on all the tyrosines (mono-, di- or tri-sulfated peptides, 7 combinations). The impact of both distribution and position of sulfate groups on the interaction between P38 and SDF-1α was studied by affinity capillary electrophoresis (ACE) hyphenated to electrospray mass spectrometry (ESI-MS).An interaction between P38 and SDF-1α was highlighted by ACE. It was strongly enhanced by the increase of P38 sulfation degree. The complex stoichiometry was then determined by ACE-MS, and 1:1 complexes were predominantly obtained, with all the peptides. This work opens the orad to the three-partner interaction studies involving glycosaminoglycans.
Advisors/Committee Members: Gonnet, Florence (thesis director).
Subjects/Keywords: SDF-1
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APA (6th Edition):
Fumex, M. (2018). Etude de la sulfatation des protéines dans les processus d’interactions biologiques : cas du récepteur aux chimiokines CXCR4 : Role of protein sulfation in biomolecular interactions : focus on the chemokine receptor CXCR4. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2018SACLE033
Chicago Manual of Style (16th Edition):
Fumex, Maud. “Etude de la sulfatation des protéines dans les processus d’interactions biologiques : cas du récepteur aux chimiokines CXCR4 : Role of protein sulfation in biomolecular interactions : focus on the chemokine receptor CXCR4.” 2018. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed March 07, 2021.
http://www.theses.fr/2018SACLE033.
MLA Handbook (7th Edition):
Fumex, Maud. “Etude de la sulfatation des protéines dans les processus d’interactions biologiques : cas du récepteur aux chimiokines CXCR4 : Role of protein sulfation in biomolecular interactions : focus on the chemokine receptor CXCR4.” 2018. Web. 07 Mar 2021.
Vancouver:
Fumex M. Etude de la sulfatation des protéines dans les processus d’interactions biologiques : cas du récepteur aux chimiokines CXCR4 : Role of protein sulfation in biomolecular interactions : focus on the chemokine receptor CXCR4. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2018. [cited 2021 Mar 07].
Available from: http://www.theses.fr/2018SACLE033.
Council of Science Editors:
Fumex M. Etude de la sulfatation des protéines dans les processus d’interactions biologiques : cas du récepteur aux chimiokines CXCR4 : Role of protein sulfation in biomolecular interactions : focus on the chemokine receptor CXCR4. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2018. Available from: http://www.theses.fr/2018SACLE033

University of Rochester
2.
Niswander, Lisa Madalen.
Microenvironmental Regulation of Megakaryopoiesis and
Thrombopoiesis by SDF-1.
Degree: PhD, 2014, University of Rochester
URL: http://hdl.handle.net/1802/28486
► Thrombocytopenia complicates many diseases and can be a life-threatening consequence of genotoxic treatments such as chemotherapy and radiation therapy, which injure bone marrow cells including…
(more)
▼ Thrombocytopenia complicates many diseases and can
be a life-threatening
consequence of genotoxic treatments such as
chemotherapy and radiation therapy,
which injure bone marrow cells
including the platelet-producing megakaryocyte (MK)
lineage. There
has been much interest in elucidating the processes of
megakaryopoiesis and thrombopoiesis in order to develop new
therapeutic strategies for
thrombocytopenia. However, the study of
primary megakaryocytes is complicated by
their low frequency in
the bone marrow and technical challenges presented by their
unique
maturation properties. To address this, we first developed and
validated an
assay utilizing imaging flow cytometry, which
combines the morphometric capabilities of
microscopy with the high
throughput analyses of flow cytometry, for efficient
quantification and characterization of the full spectrum of
maturing MKs in primary
murine bone marrow. We then used this
innovative technique to interrogate the
microenvironmental
regulation of megakaryopoiesis. MK development in the bone
marrow
progresses spatially from the endosteal niche, which promotes MK
progenitor
proliferation, to the sinusoidal vascular niche, the
site of terminal maturation and
thrombopoiesis. The chemokine
SDF-1, signaling through receptor CXCR4, is
implicated in the
maturational chemotaxis of MKs toward sinusoidal vessels. Here, we
demonstrate that both intravenous administration of SDF-1 and
stabilization of
endogenous SDF-1 acutely increase MK-vasculature
association and subsequently
thrombopoiesis with no change in MK
number. In the setting of radiation injury, we find
dynamic
fluctuations in marrow SDF-1 distribution that spatially and
temporally correlate
with variations in MK niche occupancy.
Stabilization of altered SDF-1 gradients directly
affects MK
location in the marrow. Importantly, these SDF-1-mediated changes
have
functional consequences for platelet production, as the
movement of MKs away from the
vasculature decreases circulating
platelets, while MK association with the vasculature
increases
circulating platelets. Finally, we demonstrate that manipulation of
SDF-1
gradients can improve radiation-induced thrombocytopenia in
a manner additive with
earlier treatment with the cytokine
thrombopoietin. Overall, our data support the concept
that SDF-1
regulates the spatial distribution of MKs in the marrow and
consequently
circulating platelet numbers. Ultimately, the
findings presented here improve our
understanding of the
microenvironmental regulation of the MK lineage and could lead to
novel therapeutic approaches for thrombocytopenia.
Subjects/Keywords: Imaging Flow Cytometry; Megakaryocyte; Niche; SDF-1
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Niswander, L. M. (2014). Microenvironmental Regulation of Megakaryopoiesis and
Thrombopoiesis by SDF-1. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/28486
Chicago Manual of Style (16th Edition):
Niswander, Lisa Madalen. “Microenvironmental Regulation of Megakaryopoiesis and
Thrombopoiesis by SDF-1.” 2014. Doctoral Dissertation, University of Rochester. Accessed March 07, 2021.
http://hdl.handle.net/1802/28486.
MLA Handbook (7th Edition):
Niswander, Lisa Madalen. “Microenvironmental Regulation of Megakaryopoiesis and
Thrombopoiesis by SDF-1.” 2014. Web. 07 Mar 2021.
Vancouver:
Niswander LM. Microenvironmental Regulation of Megakaryopoiesis and
Thrombopoiesis by SDF-1. [Internet] [Doctoral dissertation]. University of Rochester; 2014. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1802/28486.
Council of Science Editors:
Niswander LM. Microenvironmental Regulation of Megakaryopoiesis and
Thrombopoiesis by SDF-1. [Doctoral Dissertation]. University of Rochester; 2014. Available from: http://hdl.handle.net/1802/28486

California State University – Sacramento
3.
Nguyen, Chuong Minh.
Effects of stress-induced epinephrine on stromal cell derived factor 1's recruitment of human mesenchymal stem cells.
Degree: MA, Biological Science (Stem Cell, 2012, California State University – Sacramento
URL: http://hdl.handle.net/10211.9/1589
► Cellular therapy with mesenchymal stem cells (MSC) is emerging as a promising approach in wound healing. Understanding physiologic cues that modulate MSC migration and recruitment…
(more)
▼ Cellular therapy with mesenchymal stem cells (MSC) is emerging as a promising approach in wound healing. Understanding physiologic cues that modulate MSC migration and recruitment to wound sites is critical to maximizing their clinical use. Stromal cell-derived factor
1 (
SDF-
1), has been shown to promote MSC chemotactic migration and thus could potentially enhance wound healing. On the other hand, stress-induced epinephrine, whose systemic level can be up to 10-fold elevated in stressed patients, and is generated within the wound, has been shown to impair wound healing. The purpose of this study was to evaluate how stress-induced epinephrine impacts on MSC migratory response to
SDF-
1. MSC were treated with different concentrations of epinephrine, timolol (??
1/2-adrenergic receptor blocker) and/or
SDF-
1. Individual cells??? images were captured using Volocity software package and manually tracked in OpenLab software and migration rates were analyzed. Immunoblotting and Immunocytochemistry were performed using standard protocols. MSC were seeded and incubated for 36, 60, and 84 hours and stained with Calcein acetoxymethylester (AM) fluorescent dye to label viable cells and incubated at 37 °C for one hour to evaluate proliferation rates. It was our findings that
SDF-
1 and epinephrine synergistically enhanced MSC proliferation.
SDF-
1 significantly increased the migratory speed of MSC in a dose-dependent manner. Immunolocalization of actin and vinculin showed cytoskeleton reorganizations and increase in focal adhesions in MSC treated with
SDF-
1. We also found that MSC migratory speed was significantly reduced by treatment with epinephrine alone. This response was reversed when the ??
1/2AR antagonist timolol was co-incubated with the cells, demonstrating the ??AR specificity of the response. Immunoblotting demonstrated a significant decrease in phosphorylation of the ERK signaling pathway in epinephrine-treated MSC, correlating to the decreased migration. Surprisingly, co-incubation of MSC with both
SDF-
1 and epinephrine resulted in an increase the migratory speed relative to incubation with
SDF-
1 alone. This finding is important because it suggests that stress-induced high catecholamine environment at the wound site does not alter the positive effects of
SDF-
1 on MSC migration. Overall, our study sheds new light on the potential interactions between the two signaling pathways in MSC and provides initial evidence as to how they may be manipulated to improve healing.
Advisors/Committee Members: Landerholm, Thomas E..
Subjects/Keywords: Migration; Wound healing; Burns; SDF-1
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Nguyen, C. M. (2012). Effects of stress-induced epinephrine on stromal cell derived factor 1's recruitment of human mesenchymal stem cells. (Masters Thesis). California State University – Sacramento. Retrieved from http://hdl.handle.net/10211.9/1589
Chicago Manual of Style (16th Edition):
Nguyen, Chuong Minh. “Effects of stress-induced epinephrine on stromal cell derived factor 1's recruitment of human mesenchymal stem cells.” 2012. Masters Thesis, California State University – Sacramento. Accessed March 07, 2021.
http://hdl.handle.net/10211.9/1589.
MLA Handbook (7th Edition):
Nguyen, Chuong Minh. “Effects of stress-induced epinephrine on stromal cell derived factor 1's recruitment of human mesenchymal stem cells.” 2012. Web. 07 Mar 2021.
Vancouver:
Nguyen CM. Effects of stress-induced epinephrine on stromal cell derived factor 1's recruitment of human mesenchymal stem cells. [Internet] [Masters thesis]. California State University – Sacramento; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10211.9/1589.
Council of Science Editors:
Nguyen CM. Effects of stress-induced epinephrine on stromal cell derived factor 1's recruitment of human mesenchymal stem cells. [Masters Thesis]. California State University – Sacramento; 2012. Available from: http://hdl.handle.net/10211.9/1589

University of Toronto
4.
Sachewsky, Nadia.
Activating Neural Stem and Progenitor Cells to Enhance Neural Repair.
Degree: PhD, 2014, University of Toronto
URL: http://hdl.handle.net/1807/73773
► The discovery of neural stem cells in the adult brain has led to the promise of utilizing these cells to promote neural repair after injury…
(more)
▼ The discovery of neural stem cells in the adult brain has led to the promise of utilizing these cells to promote neural repair after injury or disease. Stroke is one of the leading causes of death and disability worldwide and there are currently no interventions that repair the brain following stroke. While neural stem cells and their progeny (together termed precursor cells) are activated following brain injury, this response alone is not sufficient to promote tissue repair or functional recovery. In order to enhance neural repair, it is important to characterize the neural stem cell pool, factors that stimulate neural precursors, and induce their proliferation, migration, and differentiation following injury. Herein, I have shown that adult neural precursor cell behaviour can be modulated throughout life using a number of different methods of stimulation. In considering strategies to activate endogenous neural precursor, I have elucidated the mechanism by which the pro-survival factor Cyclosporin A (CsA) affects enhanced neural precursor survival, specifically by inhibition of mitochondrial permeability transition pore formation. Furthermore, I considered the limitations of aging in the brain and have demonstrated that the old age brain can, in fact, respond to CsA in the same manner as was shown to enhance tissue regeneration and functional recovery in young adult mice. Subsequently, given the pro-survival effects of CsA, I have explored endogenous survival factors present in the developing brain to determine whether the adult neural precursor population can be modified by activating signaling pathways seen in development. I have shown that adult neural stem cells remain responsive both in vitro and in vivo to stromal cell-derived factor -1α (
SDF-1α) and stem cell factor (SCF) released from embryonic neurons during development. Finally, I have identified a novel population of stem cells that retain characteristics of primitive neural stem cells, which were thought to disappear during development. I have characterized this rare population of primitive neural stem cells in the adult brain showing they are responsive to leukemia inhibitory factor (LIF); they express the pluripotency marker Oct4, and they give rise to the definitive, well characterized neural stem cell in the adult brain. Significantly, these adult primitive neural stem cells respond to stroke injury by proliferating to effectively increase the size of the primitive neural stem cell pool, further suggesting that this cell population may be a target for regenerative strategies. Together, these findings provide insights into the factors that modify neural precursor pools towards the goal of developing novel stem cell based strategies for neural repair.
Advisors/Committee Members: Morshead, Cindi M, Medical Science.
Subjects/Keywords: CsA; LIF; neural stem cells; SCF; SDF-1; stroke; 0306
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Sachewsky, N. (2014). Activating Neural Stem and Progenitor Cells to Enhance Neural Repair. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/73773
Chicago Manual of Style (16th Edition):
Sachewsky, Nadia. “Activating Neural Stem and Progenitor Cells to Enhance Neural Repair.” 2014. Doctoral Dissertation, University of Toronto. Accessed March 07, 2021.
http://hdl.handle.net/1807/73773.
MLA Handbook (7th Edition):
Sachewsky, Nadia. “Activating Neural Stem and Progenitor Cells to Enhance Neural Repair.” 2014. Web. 07 Mar 2021.
Vancouver:
Sachewsky N. Activating Neural Stem and Progenitor Cells to Enhance Neural Repair. [Internet] [Doctoral dissertation]. University of Toronto; 2014. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1807/73773.
Council of Science Editors:
Sachewsky N. Activating Neural Stem and Progenitor Cells to Enhance Neural Repair. [Doctoral Dissertation]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/73773

University of Minnesota
5.
Glass, Tiffany.
Impacts of SDF-1 and radiation dose-rate in an adult zebrafish model of hematopoietic cell transplant.
Degree: PhD, Molecular, Cellular, Developmental Biology and Genetics, 2013, University of Minnesota
URL: http://purl.umn.edu/155722
► Despite a history of refinements, Hematopoietic Cell Transplant (HCT) remains a potentially difficult treatment that can have high risks for complications and mortality. We used…
(more)
▼ Despite a history of refinements, Hematopoietic Cell Transplant (HCT) remains a
potentially difficult treatment that can have high risks for complications and
mortality. We used adult zebrafish models of HCT to study two broad biological
processes that occur during HCT; homing and early donor-derived hematopoietic
reconstitution. In the first case, we validated the adult zebrafish model for the
study of the chemokine SDF-1 in HCT, developed a transgenic sdf-1 reporter
zebrafish line, and used it to determine sites of high sdf-1 expression in recipient
organisms. These sites were discovered both in the hematopoietic tissue as well
as in previously un-described structures throughout the skin, and were found to
consistently attract donor-derived cells after transplant. Ultimately, this allowed
the identification of new putative HSC-niche cells which can be isolated with
relative ease. Secondly, we assessed the effects of high conditioning radiation
dose-rates on the process of hematopoietic engraftment after transplant. In
groups of adult zebrafish given the same total dose of preconditioning radiation,
we found that recipients irradiated at a high rate show significantly faster
engraftment compared to those irradiated at a lower rate. Insights offered by this
work will contribute to future efforts identifying endogenous factors promoting
rapid engraftment, as well as to future reassessments of therapeutic opportunities offered by biologically informed refinements of preconditioning
radiation strategies.
Subjects/Keywords: CXCL12; Hematopoietic cell transplant; Radiation; SDF-1; Zebrafish
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Glass, T. (2013). Impacts of SDF-1 and radiation dose-rate in an adult zebrafish model of hematopoietic cell transplant. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/155722
Chicago Manual of Style (16th Edition):
Glass, Tiffany. “Impacts of SDF-1 and radiation dose-rate in an adult zebrafish model of hematopoietic cell transplant.” 2013. Doctoral Dissertation, University of Minnesota. Accessed March 07, 2021.
http://purl.umn.edu/155722.
MLA Handbook (7th Edition):
Glass, Tiffany. “Impacts of SDF-1 and radiation dose-rate in an adult zebrafish model of hematopoietic cell transplant.” 2013. Web. 07 Mar 2021.
Vancouver:
Glass T. Impacts of SDF-1 and radiation dose-rate in an adult zebrafish model of hematopoietic cell transplant. [Internet] [Doctoral dissertation]. University of Minnesota; 2013. [cited 2021 Mar 07].
Available from: http://purl.umn.edu/155722.
Council of Science Editors:
Glass T. Impacts of SDF-1 and radiation dose-rate in an adult zebrafish model of hematopoietic cell transplant. [Doctoral Dissertation]. University of Minnesota; 2013. Available from: http://purl.umn.edu/155722

Université Paris-Sud – Paris XI
6.
Barry Delongchamps, Nicolas.
Mécanismes de progression des carcinomes de la prostate et recherche de nouveaux facteurs pronostiques : Progression Mechanisms of Prostate Cancer and New Prognostic Factors.
Degree: Docteur es, Cancérologie, 2013, Université Paris-Sud – Paris XI
URL: http://www.theses.fr/2013PA11T011
► Parallèlement au rôle central du récepteur aux androgènes, l’environnement tumoral immédiat exerce aussi une action majeure sur la progression du cancer de la prostate. L’hypoxie…
(more)
▼ Parallèlement au rôle central du récepteur aux androgènes, l’environnement tumoral immédiat exerce aussi une action majeure sur la progression du cancer de la prostate. L’hypoxie locale, par le biais de régulations multiples, serait impliquée dans la migration cellulaire et la dissémination tumorale. L’objectif de ma thèse a été d’identifier de nouvelles cibles thérapeutiques et de nouveaux marqueurs pronostiques pour ces cancers. J’ai tout d’abord participé à l’identification d’un partenaire du récepteur aux androgènes, la protéine CAD, enzyme clé de la synthèse des pyrimidines. Parallèlement, nous nous sommes intéressés au rôle d’un anti-angiogénique endogène dans la progression du cancer de la prostate, la thrombospondine-1 (TSP-1). Bien que l’activité anti angiogénique soit souvent considérée comme anti-tumorale, nous avons mis en évidence le caractère protumoral de la TSP-1, par son action promigratoire sur les cellules tumorales. Ces travaux m’ont conduits à étudier l’axe CXCR4/SDF-1, régulé en partie par l’hypoxie et stimulant la migration cellulaire. Nous avons montré sur tissu humain que CXCR4 était exprimé principalement au niveau du front tumoral des cancers localisés et localement avancés, et que son expression était associée à une transition épithélio-mésenchymateuse. SDF-1 était surexprimée selon un gradient croissant allant du centre des tumeurs vers le tissu péritumoral distant, exerçant possiblement un chimiotactisme sur les cellules du front tumoral. La surexpression de CXCR4 au front tumoral ainsi que le gradient de SDF1 étaient associés au pronostic.
In addition to the pivotal role of the androgen receptor, the immediate tumor microenvironment plays an essential role in prostate cancer progression. Local hypoxia, through multiple regulation mechanisms, may be implicated in the migration of tumor cells and dissemination. The aim of my thesis was to identify new therapeutic targets and prognostic markers for these cancers. I first participated in the identification of a new partner of the androgen receptor, the protein CAD that is a key enzyme of pyrimidine synthesis. We also studied the role of the endogenous anti-angiogenic thrombospondin-1 (TSP-1) in prostate cancer progression. Although anti-angiogenic activity is usually matched with tumor inhibition, we showed that TSP-1 exerted protumoral effects by stimulating cell migration. These observations led me to study the hypoxia-induced CXCR4/SDF-1 axis that is known to promote cell migration through the extra-cellular matrix. We showed on human tissue that CXCR4 was overexpressed in the tumor front of localized and locally advanced prostate cancers, and that its expression was associated with an epithelial mesenchymal transition. An increasing gradient of SDF-1 was observed from the tumor center to the distant peritumoral tissue, potentially attracting CXCR4-expressing tumor cells of the tumor front. CXCR4 overexpression in the tumor front, as well as SDF1 gradient, were associated with prognosis.
Advisors/Committee Members: Cabon, Florence (thesis director).
Subjects/Keywords: Cancer de la prostate; CAD; Angiogenèse; TSP-1; CXCR4; SDF-1; Pronostic; Prostate cancer; CAD; Angiogenesis; TSP-1; Cxcr4; SDF-1; Prognosis
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Barry Delongchamps, N. (2013). Mécanismes de progression des carcinomes de la prostate et recherche de nouveaux facteurs pronostiques : Progression Mechanisms of Prostate Cancer and New Prognostic Factors. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2013PA11T011
Chicago Manual of Style (16th Edition):
Barry Delongchamps, Nicolas. “Mécanismes de progression des carcinomes de la prostate et recherche de nouveaux facteurs pronostiques : Progression Mechanisms of Prostate Cancer and New Prognostic Factors.” 2013. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed March 07, 2021.
http://www.theses.fr/2013PA11T011.
MLA Handbook (7th Edition):
Barry Delongchamps, Nicolas. “Mécanismes de progression des carcinomes de la prostate et recherche de nouveaux facteurs pronostiques : Progression Mechanisms of Prostate Cancer and New Prognostic Factors.” 2013. Web. 07 Mar 2021.
Vancouver:
Barry Delongchamps N. Mécanismes de progression des carcinomes de la prostate et recherche de nouveaux facteurs pronostiques : Progression Mechanisms of Prostate Cancer and New Prognostic Factors. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2013. [cited 2021 Mar 07].
Available from: http://www.theses.fr/2013PA11T011.
Council of Science Editors:
Barry Delongchamps N. Mécanismes de progression des carcinomes de la prostate et recherche de nouveaux facteurs pronostiques : Progression Mechanisms of Prostate Cancer and New Prognostic Factors. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2013. Available from: http://www.theses.fr/2013PA11T011
7.
Liarmakopoulos, Emmanouil.
Παράγοντες του στρώματος του όγκου και αποπτωτικά μόρια στον γαστρικό καρκίνο.
Degree: 2019, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)
URL: http://hdl.handle.net/10442/hedi/46793
► Background : Caspase-8 and caspase-9 (CASP9) are protease enzymes that play essential roles in regulating apoptosis. Stromal-cell derived factor-1 (SDF-1), a CXC chemokine, is important…
(more)
▼ Background : Caspase-8 and caspase-9 (CASP9) are protease enzymes that play essential roles in regulating apoptosis. Stromal-cell derived factor-1 (SDF-1), a CXC chemokine, is important for growth, angiogenesis and metastasis of tumor cells. Survivin is a member of the inhibitor of apoptosis family of proteins. E-selectin is an adhesion molecule expressed on activated endothelial cells and plays an important role in the mechanism of cancer metastasis, regulating the adhesion of circulating cancer cells to the blood vessels. Our aim was to investigate the association of these molecules most common gene polymorphisms with gastric cancer (GC) susceptibility. Methods : We performed a case-control study of 88 gastric cancer cases and 480 controls to analyze the association between CASP8 -652 6N ins/del, CASP9 -1263 A>G, SDF1-3'A, survivin promoter -31G/C and E-selectin S128R gene polymorphisms and GC susceptibility. The genotyping analysis was done by Polymerase chain reaction -restriction fragment length polymorphism method. Results : CASP8 -652 6N ins/del polymorphism and CASP9 -1263 GG genotype were observed to be significantly associated with a lower risk of gastric cancer. Both CASP8 del/del and CASP9 -1263 GG genotypes were associated with increased overall survival in gastric cancer patients. The SDF1-3'A genotype frequencies for GG, GA and AA were 44.32, 48.86 and 6.92% in patients and 42.71, 47.71 and 9.58% in healthy subjects, respectively. GA+AA genotype frequency and A allele distribution were not identified as significantly different between gastric cancer cases and controls. The survivin frequencies for GG, GC and CC were 20.45, 50 and 29.54% in patients and 33.96, 45 and 21.04% in control group, respectively. The C carriers (GC+CC genotype) and the C allele were over-represented among the gastric cancer cases (P=0.013 and P=0.0083, respectively). The E-selectin S128R C allele, CA and CC genotypes were over-represented among the GC cases. However, carrying the C allele was associated with poor survival.No statistically significant association was observed between all the above polymorphisms and tumor characteristics. Conclusions : The CASP8 -652 6N ins/del and the CASP9 -1263 A>G polymorphisms were observed to play a protective role in GC predisposition. The survivin promoter -31G/C polymorphism may confer an increased susceptibility to gastric cancer, while the SDF1-3'A polymorphism may not be a candidate genetic variant to select individuals at higher risk of developing gastric cancer. The E-selectin S128R C allele may confer an increased susceptibility to gastric cancer development and correlate with a poor prognosis.
Εισαγωγή – Σκοπός: Οι κασπάσες -8 και -9, διαδραματίζουν σημαντικό ρόλο στην ρύθμιση της απόπτωσης. Ο προερχόμενος από το στρώμα παράγοντας 1 (SDF-1), μέλος της οικογένειας χημειοκινών CXC, είναι σημαντικός για την ανάπτυξη, την αγγειογένεση και την μετάσταση των καρκινικών κυττάρων. Η σουρβιβίνη αποτελεί μέλος της οικογένειας των αναστολέων της απόπτωσης (IAPs). Η Ε-σελεκτίνη είναι ένα…
Subjects/Keywords: Κασπάσης -8; E-σελεκτίνη; Κασπάσης -9; Σουρβιβίνη; Πολυμορφισμοί; Caspase-8 CASP8; Caspase-9 CASP9; Stromal-cell derived factor-1 SDF-1; E-selectin; Survivin; Polymorphism; SDF-1
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Liarmakopoulos, E. (2019). Παράγοντες του στρώματος του όγκου και αποπτωτικά μόρια στον γαστρικό καρκίνο. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/46793
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Liarmakopoulos, Emmanouil. “Παράγοντες του στρώματος του όγκου και αποπτωτικά μόρια στον γαστρικό καρκίνο.” 2019. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed March 07, 2021.
http://hdl.handle.net/10442/hedi/46793.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Liarmakopoulos, Emmanouil. “Παράγοντες του στρώματος του όγκου και αποπτωτικά μόρια στον γαστρικό καρκίνο.” 2019. Web. 07 Mar 2021.
Vancouver:
Liarmakopoulos E. Παράγοντες του στρώματος του όγκου και αποπτωτικά μόρια στον γαστρικό καρκίνο. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10442/hedi/46793.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Liarmakopoulos E. Παράγοντες του στρώματος του όγκου και αποπτωτικά μόρια στον γαστρικό καρκίνο. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. Available from: http://hdl.handle.net/10442/hedi/46793
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
8.
Oliveira, Adriana Morgan de.
Expressão da quimiocina SDF-1, (CXCL12) e seu respectivo receptor CXCR4 em células de pacientes com mieloma múltiplo em linhagem de células mieloma múltiplo humano (RPMI-8226) após tratamento com talidomida.
Degree: Mestrado, Fisiopatologia Experimental, 2008, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/5/5160/tde-30102008-145739/
;
► Mieloma Múltiplo é a segunda doença com maior prevalência nas doenças malignidades hematológica, incurável com média de sobrevivência de 3-5 anos. MM é uma malignidade…
(more)
▼ Mieloma Múltiplo é a segunda doença com maior prevalência nas doenças malignidades hematológica, incurável com média de sobrevivência de 3-5 anos. MM é uma malignidade das células do plasma caracterizada pela destruição e reabsorção óssea e supressão da formação do osso. A quimiocina SDF-1 (CXCL12) e seu receptor CXCR4 têm um importante papel direcional na migração, homing das células do plasma em mieloma múltiplo e mobilização das células de MM para fora da medula óssea. A talidomida tem sido usada com êxito no tratamento de pacientes com mieloma múltiplo. Neste estudo verificamos o efeito da talidomida na expressão da quimiocina SDF-1 e seu receptor CXCR4 em pacientes com mieloma múltiplo e em linhagem de células de mieloma múltiplo humano (RPMI-8226) tratados e sem tratamento de talidomida. Nossos resultamos mostraram uma expressão heterogênea na expressão da quimiocina SDF-1 e seu receptor CXCR4 nos pacientes com mieloma múltiplo estudado (n= 79). Entretanto, pacientes com mieloma múltiplo tratados com talidomida mostraram uma baixa expressão da quimiocina SDF-1 e seu receptor CXC4 quando comparados com pacientes recém diagnosticados para mieloma múltiplo e pacientes com mieloma múltiplo tratados com outros medicamentos. Nossos resultados sugerem que o tratamento com talidomida induz uma baixa regulação na expressão no ligante SDF-1 e seu receptor CXCR4 em pacientes com mieloma múltiplo
Multiple Myeloma (MM) is a second most prevalent hematological malignancy and remains incurable with a median survival of 3-5 years. MM is a plasma cell malignancy characterized by devastating bone destruction due to the enhanced bone resorption and suppressed bone formation. The chemokine stromal-derived factor-1 (SDF-1) and its receptor CXCR4 play an important role in directional migration, homing of plasma cells in multiple myeloma (MM) and mobilization of MM cells out of the bone marrow. The drug thalidomide has been successfully used in the treatment of patients with MM. In this study, we assessed the effect of thalidomide on SDF-1 and CXCR4 expression in MM patients and human myeloma-derived cell line, RPMI 8226 treated with or without thalidomide. A heterogeneous expression pattern of chemokines SDF-1 and CXCR4 receptor were observed for all MM patients studied. However, patients treated with thalidomide showed a significantly decrease in expression of SDF-1 and CXCR4 as compared to newly diagnosed MM patients and MM patients treated with other drugs. RPMI 8226 cell line treated with 10, 20 and 100µM thalidomide also demonstrated decrease in SDF-1 and CXCR4 expression as compared with cell control (RPMI-8226 without thalidomide). Ours results indicate that thalidomide therapy induces down-regulation of CXCR4 and its ligand SDF-1 in multiple myeloma
Advisors/Committee Members: Novak, Estela Maria.
Subjects/Keywords: Chemokine SDF-1 and CXCR4 receptor; Linhagem de células RPMI-8226; Mieloma múltiplo; Multiple myeloma; Quimiocinas SDF-1/ CXCR4; RPMI-8226 cell line; Talidomida; Thalidomide
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Oliveira, A. M. d. (2008). Expressão da quimiocina SDF-1, (CXCL12) e seu respectivo receptor CXCR4 em células de pacientes com mieloma múltiplo em linhagem de células mieloma múltiplo humano (RPMI-8226) após tratamento com talidomida. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5160/tde-30102008-145739/ ;
Chicago Manual of Style (16th Edition):
Oliveira, Adriana Morgan de. “Expressão da quimiocina SDF-1, (CXCL12) e seu respectivo receptor CXCR4 em células de pacientes com mieloma múltiplo em linhagem de células mieloma múltiplo humano (RPMI-8226) após tratamento com talidomida.” 2008. Masters Thesis, University of São Paulo. Accessed March 07, 2021.
http://www.teses.usp.br/teses/disponiveis/5/5160/tde-30102008-145739/ ;.
MLA Handbook (7th Edition):
Oliveira, Adriana Morgan de. “Expressão da quimiocina SDF-1, (CXCL12) e seu respectivo receptor CXCR4 em células de pacientes com mieloma múltiplo em linhagem de células mieloma múltiplo humano (RPMI-8226) após tratamento com talidomida.” 2008. Web. 07 Mar 2021.
Vancouver:
Oliveira AMd. Expressão da quimiocina SDF-1, (CXCL12) e seu respectivo receptor CXCR4 em células de pacientes com mieloma múltiplo em linhagem de células mieloma múltiplo humano (RPMI-8226) após tratamento com talidomida. [Internet] [Masters thesis]. University of São Paulo; 2008. [cited 2021 Mar 07].
Available from: http://www.teses.usp.br/teses/disponiveis/5/5160/tde-30102008-145739/ ;.
Council of Science Editors:
Oliveira AMd. Expressão da quimiocina SDF-1, (CXCL12) e seu respectivo receptor CXCR4 em células de pacientes com mieloma múltiplo em linhagem de células mieloma múltiplo humano (RPMI-8226) após tratamento com talidomida. [Masters Thesis]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/5/5160/tde-30102008-145739/ ;
9.
Bordenave, Jennifer.
Role des Péricytes Pulmonaires dans l’Hypertension Artérielle Pulmonaire : à la recherche de nouvelles cibles thérapeutiques : Role of pericytes pulmonary in Pulmonary arterial hypertension : in search of new therapeutic targets.
Degree: Docteur es, Physiologie, physiopathologie, 2019, Université Paris-Saclay (ComUE)
URL: http://www.theses.fr/2019SACLS294
► Les péricytes sont fortement suspectés de jouer un rôle déterminant dans la physiopathologie de l’hypertension artérielle pulmonaire (HTAP), non seulement en raison de leur position…
(more)
▼ Les péricytes sont fortement suspectés de jouer un rôle déterminant dans la physiopathologie de l’hypertension artérielle pulmonaire (HTAP), non seulement en raison de leur position et distribution, de leur rôle dans l'homéostasie vasculaire, de leur plasticité et spécificité tissulaire, mais aussi vu leur nette augmentation en nombre autour des artérioles pulmonaires remodelées. Cependant, les mécanismes impliqués dans leur accumulation autour des vaisseaux remodelés ainsi que leur importance dans la mise en place et la progression de l’HTAP restent encore incompris. De plus, nous ne savons pas si les péricytes présentent ou non des anomalies phénotypiques dans l’HTAP.C’est pourquoi ces travaux de doctorat ont visé à : 1) Identifier les possibles anomalies intrinsèques des péricytes provenant de patients HTAP ; 2) Préciser rôle de la voie de signalisation CXCL12/CXCR4/CXCR7 dans l’augmentation de la couverture péricytaire et tester des inhibiteurs de cette voie dans des modèles précliniques d’hypertension pulmonaire (HP) ; 3) Etudier l’impact du pouvoir mésenchymateux des péricytes dans le remodelage vasculaire pulmonaire associé à l’HTAP.Nos données ont permis d’une part de démontrer que les péricytes provenant de patients HTAP possédent des défauts intrinsèques dans les mécanismes de prolifération, de migration et de différenciation cellulaire et que la voie du CXCL12 contribue fortement à l’augmentation anormale de la couverture péricytaire autour des vaisseaux remodelés de patients HTAP. D’autre part, via leur capacité à se différencier en cellules contractiles, nous avons pu démontrer que les péricytes contribuaient directement au remodelage vasculaire pulmonaire.En conclusion, notre étude montre ainsi l’importance du rôle des péricytes pulmonaires dans la progression de l’hypertension artérielle pulmonaire humaine et expérimentale.
Pericytes (PCs) are strongly suspected to play a determining role in the pathophysiology of pulmonary arterial hypertension (PAH), because of their position and distribution, role in vascular homeostasis, versatility and tissue-specificity, but also because they accumulate around remodeled pulmonary arterioles in PAH. However, the underlying mechanisms and their dynamic role in PAH are still unknown. Furthermore, we do not know whether pulmonary PCs are phenotypically and functionally altered in PAH. To answer these questions, our objective were: 1) To examine the phenotypic and functional characteristics of human pulmonary PCs derived from control and PAH patients; 2) To precise the role of the intrinsic abnormalities in the altered phenotype of pulmonary PCs in PAH; 3) To study the dynamic role(s) of pulmonary PCs in preclinical PAH models, especially through modulation of the CXCL12/CXCR4/CXCR7 signaling pathway. Taken together, our findings identify for the first time phenotypic and functional abnormalities of pulmonary PCs in PAH with pathogenetic significance since they increased directly their proliferation, migration and capacity to differentiate in smooth muscle-like…
Advisors/Committee Members: Guignabert, Christophe (thesis director), Tu, Ly (thesis director).
Subjects/Keywords: Hypertension pulmonaire; Péricyte; Remodelage vasculaire pulmonaire; Sdf-1; Progéniteurs mésenchymateux; Lignage cellulaire; Pulmonary hypertension; Pericyte; Pulmonary vascular remodeling; Sdf-1; Mesenchymal progenitors; Lineage tracing
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bordenave, J. (2019). Role des Péricytes Pulmonaires dans l’Hypertension Artérielle Pulmonaire : à la recherche de nouvelles cibles thérapeutiques : Role of pericytes pulmonary in Pulmonary arterial hypertension : in search of new therapeutic targets. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2019SACLS294
Chicago Manual of Style (16th Edition):
Bordenave, Jennifer. “Role des Péricytes Pulmonaires dans l’Hypertension Artérielle Pulmonaire : à la recherche de nouvelles cibles thérapeutiques : Role of pericytes pulmonary in Pulmonary arterial hypertension : in search of new therapeutic targets.” 2019. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed March 07, 2021.
http://www.theses.fr/2019SACLS294.
MLA Handbook (7th Edition):
Bordenave, Jennifer. “Role des Péricytes Pulmonaires dans l’Hypertension Artérielle Pulmonaire : à la recherche de nouvelles cibles thérapeutiques : Role of pericytes pulmonary in Pulmonary arterial hypertension : in search of new therapeutic targets.” 2019. Web. 07 Mar 2021.
Vancouver:
Bordenave J. Role des Péricytes Pulmonaires dans l’Hypertension Artérielle Pulmonaire : à la recherche de nouvelles cibles thérapeutiques : Role of pericytes pulmonary in Pulmonary arterial hypertension : in search of new therapeutic targets. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2019. [cited 2021 Mar 07].
Available from: http://www.theses.fr/2019SACLS294.
Council of Science Editors:
Bordenave J. Role des Péricytes Pulmonaires dans l’Hypertension Artérielle Pulmonaire : à la recherche de nouvelles cibles thérapeutiques : Role of pericytes pulmonary in Pulmonary arterial hypertension : in search of new therapeutic targets. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2019. Available from: http://www.theses.fr/2019SACLS294

Université Paris-Sud – Paris XI
10.
Nasreddine, Salam.
Etude de deux chimiokines CXCL12/SDF-1 et fractalkine (FKN)/CX3CL1 dans le cancer épithélial des ovaires : Study of the two chemokines CXCL12/SDF-1 and fractalkine (FKN)/CX3CL1 in epithelial ovarian cancer (EOC).
Degree: Docteur es, Immunologie, 2011, Université Paris-Sud – Paris XI
URL: http://www.theses.fr/2011PA11T019
► Le cancer épithélial de l’ovaire (CEO) est une cause majeure de mortalité parcancer gynécologique. Il est associé à un mauvais pronostic car il est souventdécouvert…
(more)
▼ Le cancer épithélial de l’ovaire (CEO) est une cause majeure de mortalité parcancer gynécologique. Il est associé à un mauvais pronostic car il est souventdécouvert à un stade tardif. Mieux comprendre les causes et les mécanismesmoléculaires et cellulaires associés à la progression de ce cancer représente unenjeu majeur.Les deux chimiokines CXCL12/SDF-1 et fractalkine (FKN)/CX3CL1 ont étéimpliquées dans diverses tumeurs. La chimiokine SDF-1, a un effetimmunosuppresseur dans le CEO. Elle est aussi impliquée dans l’angiogenèsetumorale. L’effet de SDF-1 médié par CXCR4 est également impliqué dans larégulation de la prolifération, la survie, la migration et l'invasion des cellulescancéreuses. La FKN, a largement été mise en évidence dans les tissusépithéliaux et dans divers cancers où elle peut avoir soit un rôle anti-tumoral soitun rôle pro-tumoral. Jusqu’à présent la FKN n’a pas été étudié dans le CEO.Dans notre étude, nous avons démontré l’expression de SDF-1 et de la FKNdans l’épithélium de surface de l’ovaire sain et dans les tumeurs bénignes etmalignes. Ces résultats montrent que l’expression de SDF-1 et de la FKNpréexiste à la tumorigenèse. Nous avons démontré une expression hétérogènedes deux chimiokines dans les cellules du CEO. Les niveaux d’expression deSDF-1 dans les cellules tumorales sur une cohorte de 183 patientes n’ont aucunevaleur pronostique sur la survie globale et sur la survie sans progressiontumorale des patientes atteintes par le CEO. L’étude de la corrélation del’expression de la FKN avec les deux marqueurs de prolifération, Ki-67 etGILZ, sur une autre cohorte de 54 patientes, complétée par des expériences invitro, a montré que GILZ augmente l’expression de la FKN et d’autre part que laFKN elle-même augmente la prolifération. Cette étude contribue à élucider lerôle de SDF-1 et de la FKN dans le CEO.
Little is known about the molecules that contribute to tumor growth ofepithelial ovarian carcinomas (EOC) that remains the most lethal gynecologicalneoplasm in women.The two chemokines CXCL12/SDF-1 and fractalkine (FKN)/CX3CL1 havebeen widely studied in tumorigenesis. In epithelial ovarian cancer (EOC), SDF-1enhances tumor angiogenesis and contributes to the immunosuppressivenetwork. SDF-1 also acts on tumor cell proliferation and survival and, throughits main receptor CXCR4, governs the migration of malignant cells and theirinvasion of the peritoneum. The chemokine FKN has been documented inepithelial tissues and in various cancers. FKN have paradoxical effects intumors: anti-tumoral effect in some tumor entities and pro-tumoral effect inother tumor entities.In our study, we demonstrated the expression of SDF-1 and FKN on thesurface epithelium of normal ovaries and benign and malignant tumors,suggesting that the expression of these chemokines preexists to tumorigenesis.We also demonstrated an heterogeneous expression of both chemokines in EOC.In our large and homogeneous cohort (183 specimens of EOC), SDF-1expression levels had no effect on overall survival or progression-free survival.Thus, SDF-1…
Advisors/Committee Members: Machelon, Véronique (thesis director).
Subjects/Keywords: Cancer épithélial de l’ovaire; CXCL12/SDF-1; Valeur pronostique; Fractalkine (FKN)/CX3CL1; GILZ; Prolifération; Epithelial ovarian cancer; CXCL12/SDF-1; Prognostic value; Fractalkine (FKN)/CX3CL1; GILZ; Proliferation
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Nasreddine, S. (2011). Etude de deux chimiokines CXCL12/SDF-1 et fractalkine (FKN)/CX3CL1 dans le cancer épithélial des ovaires : Study of the two chemokines CXCL12/SDF-1 and fractalkine (FKN)/CX3CL1 in epithelial ovarian cancer (EOC). (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2011PA11T019
Chicago Manual of Style (16th Edition):
Nasreddine, Salam. “Etude de deux chimiokines CXCL12/SDF-1 et fractalkine (FKN)/CX3CL1 dans le cancer épithélial des ovaires : Study of the two chemokines CXCL12/SDF-1 and fractalkine (FKN)/CX3CL1 in epithelial ovarian cancer (EOC).” 2011. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed March 07, 2021.
http://www.theses.fr/2011PA11T019.
MLA Handbook (7th Edition):
Nasreddine, Salam. “Etude de deux chimiokines CXCL12/SDF-1 et fractalkine (FKN)/CX3CL1 dans le cancer épithélial des ovaires : Study of the two chemokines CXCL12/SDF-1 and fractalkine (FKN)/CX3CL1 in epithelial ovarian cancer (EOC).” 2011. Web. 07 Mar 2021.
Vancouver:
Nasreddine S. Etude de deux chimiokines CXCL12/SDF-1 et fractalkine (FKN)/CX3CL1 dans le cancer épithélial des ovaires : Study of the two chemokines CXCL12/SDF-1 and fractalkine (FKN)/CX3CL1 in epithelial ovarian cancer (EOC). [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2011. [cited 2021 Mar 07].
Available from: http://www.theses.fr/2011PA11T019.
Council of Science Editors:
Nasreddine S. Etude de deux chimiokines CXCL12/SDF-1 et fractalkine (FKN)/CX3CL1 dans le cancer épithélial des ovaires : Study of the two chemokines CXCL12/SDF-1 and fractalkine (FKN)/CX3CL1 in epithelial ovarian cancer (EOC). [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2011. Available from: http://www.theses.fr/2011PA11T019

Freie Universität Berlin
11.
Ghadge, Santhosh Kumar.
Kardiomyozytenspezifische Ablation von stromal cell derived factor-1
(SDF-1/CXCL12) schützt vor Schädigung des Herzens unter Hypertrophie und
Ischämiebedingungen.
Degree: 2011, Freie Universität Berlin
URL: https://refubium.fu-berlin.de/handle/fub188/10532
► Die Wirksamkeit von Stammzell-basierten Therapieansätzen konnte mit der Mobilisierung der Stammzellen zu geschädigtem Herzgewebe nach Myokardinfarkt (MI) gezeigt werden. Der Prozess der Stammzellmobilisierung wird dabei…
(more)
▼ Die Wirksamkeit von Stammzell-basierten Therapieansätzen konnte mit der
Mobilisierung der Stammzellen zu geschädigtem Herzgewebe nach Myokardinfarkt
(MI) gezeigt werden. Der Prozess der Stammzellmobilisierung wird dabei durch
das entzündete oder verletzte Gewebe ausgelöst, indem verschiedene
Signalmoleküle wie Zytokine, Chemokine und proteolytische Enzyme freigesetzt
werden. Vor allem die Chemokine nehmen eine entscheidende Rolle in der
Pathophysiologie von ischämischen Verletzungen ein. Das Chemokin
SDF-
1 ist
dabei von zentraler Bedeutung in der Regulierung der Mobilisierung von Stamm-
und Vorläuferzellen und ist besonders wichtig für die Regeneration des Herzens
nach Myokardinfarkt durch Anregung von Angiogenese sowie durch Verstärkung
protektiver Mechanismen. Deshalb wurde
SDF-1α als potentieller Angriffspunkt
für Stammzell-vermittelte kardiale Regeneration beschrieben. Dies führte sogar
zur Initiierung klinischer Studien mit Patienten, die an Ischämie-bedingten
kardialen Erkrankungen leiden. Trotz der vielfach beschriebenen positiven
Effekte des Chemokins gibt es eine Reihe von Studien, die negative
Auswirkungen der
SDF-
1/CXCR4 Achse postulieren. In der vorliegenden Arbeit
wurde ein Herz-spezifisches
SDF-
1 Knockout-Modell benutzt, um den Einfluss von
SDF-
1 auf Herzinsuffizienz sowie Myokardinfarkt zu untersuchen. Die dazu
durchgeführten in vivo Studien zeigten, dass das Fehlen von
SDF-
1 im Herz
weder zu strukturellen Auffälligkeiten noch veränderter Herzfunktion führt.
Auch nach Induzierung von kardialer Hypertrophie blieb die Herzmorphologie und
-funktion unverändert, allerdings zeigten die Knockout-Tiere eine leichte
Resistenz gegenüber dem hypertrophen Stimulus im Vergleich zu Wildtyp-
Kontrollen. Genauere Analysen ergaben, dass die Mutanten deutlich weniger
Fibrose bilden. Diese Daten deuten darauf hin, dass
SDF-
1 eine Rolle bei der
Regulierung der Herzinsuffizienz spielt. Weiterführende Experimente zeigten
zudem, dass die Herzen der Knockout-Tiere nach Auslösung eines Myokardinfarkts
besser geschützt sind als entsprechende Kontrollen. Während die Wildtyp-Tiere
stark vergrößerte diastolische und systolische Durchmesser aufwiesen, war
dieser Effekt in den Knockout-Tieren weniger stark ausgeprägt. Funktionelle
Daten sowie eine verringerte Infiltration von Entzündungszellen in den
Knockout-Mäusen bestätigten den negativen Einfluss von
SDF-
1 auf die
Herzkontraktilität nach Myokardinfarkt. Unsere Ergebnisse zeigen, dass
zukünftige mechanistische Analysen notwendig sind, um die Rolle von
SDF-
1 im
Herz nach Auftreten eines Infarkts weiter zu entschlüsseln. Zudem sollte das
therapeutische Potential von
SDF-
1 für Stammzell-basierte kardiale
Regenerationsprozesse kritisch untersucht werden.
Advisors/Committee Members: [email protected] (contact), [email protected] (contact), m (gender), Prof. Dr. Udo Heinemann (firstReferee), Prof. Dr. Michael Bader (furtherReferee).
Subjects/Keywords: SDF-1; Cardiac hypertrophy; Inflammation; Myocardial infarction; 500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ghadge, S. K. (2011). Kardiomyozytenspezifische Ablation von stromal cell derived factor-1
(SDF-1/CXCL12) schützt vor Schädigung des Herzens unter Hypertrophie und
Ischämiebedingungen. (Thesis). Freie Universität Berlin. Retrieved from https://refubium.fu-berlin.de/handle/fub188/10532
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ghadge, Santhosh Kumar. “Kardiomyozytenspezifische Ablation von stromal cell derived factor-1
(SDF-1/CXCL12) schützt vor Schädigung des Herzens unter Hypertrophie und
Ischämiebedingungen.” 2011. Thesis, Freie Universität Berlin. Accessed March 07, 2021.
https://refubium.fu-berlin.de/handle/fub188/10532.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ghadge, Santhosh Kumar. “Kardiomyozytenspezifische Ablation von stromal cell derived factor-1
(SDF-1/CXCL12) schützt vor Schädigung des Herzens unter Hypertrophie und
Ischämiebedingungen.” 2011. Web. 07 Mar 2021.
Vancouver:
Ghadge SK. Kardiomyozytenspezifische Ablation von stromal cell derived factor-1
(SDF-1/CXCL12) schützt vor Schädigung des Herzens unter Hypertrophie und
Ischämiebedingungen. [Internet] [Thesis]. Freie Universität Berlin; 2011. [cited 2021 Mar 07].
Available from: https://refubium.fu-berlin.de/handle/fub188/10532.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ghadge SK. Kardiomyozytenspezifische Ablation von stromal cell derived factor-1
(SDF-1/CXCL12) schützt vor Schädigung des Herzens unter Hypertrophie und
Ischämiebedingungen. [Thesis]. Freie Universität Berlin; 2011. Available from: https://refubium.fu-berlin.de/handle/fub188/10532
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
12.
Παπαθεοδώρου, Χαράλαμπος.
Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CΧCR4) σε πρωτοπαθή καρκινώματα μαστού.
Degree: 2011, University of Patras
URL: http://hdl.handle.net/10889/5666
► Ο καρκίνος του μαστού αποτελεί τον πιο συχνό τύπο καρκίνου των γυναικών. Παρότι η σχετική έρευνα είναι αρκετά εκτεταμένη, οι υποκείμενοι μηχανισμοί δεν έχουν πλήρως…
(more)
▼ Ο καρκίνος του μαστού αποτελεί τον πιο συχνό τύπο καρκίνου των γυναικών. Παρότι η σχετική έρευνα είναι αρκετά εκτεταμένη, οι υποκείμενοι μηχανισμοί δεν έχουν πλήρως αποσαφηνιστεί. Πρόσφατες μελέτες έχουν αναδείξει τη σημαντικότητα της διαντίδρασης των καρκινικών κυττάρων και του καρκινικού μικροπεριβάλλοντος ως μια κομβική συνιστώσα στη παθοφυσιολογίας της νόσου. Σκοπός της παρούσας μελέτης είναι η διερεύνηση της ανοσοϊστοχημικής έκφραση του υποδοχέα CXCR4, της χημοκίνης SDF-1, της μεταλλοπρωτεϊνάσης MMP-9 και του παράγοντα HIF-1α σε διηθητικά καρκινώματα του μαστού και στον παρακείμενο μη καρκινικό ιστό (τόσο στο επιθηλιακό όσο και στο στρωματικό στοιχείο), καθώς και οι συσχετίσεις των ποικίλων ανοσοεντοπίσεων με τις κλινικοπαθολογοανατομικές παραμέτρους και την επιβίωση. η επιλογή των μορίων έγινε βάσει της σημαντικότητάς τους σε ποικίλα στάδια της παθογένειας της νόσου (υποξία, νεοαγγείωση, ανάπτυξη κτλ). Η έκφραση όλων των υπό εξέταση μορίων ήταν στατιστικά σημαντικότερη στον καρκινικό ιστό σε σχέση με τον παρακείμενο μη νεοπλασματικό. Από τα αποτελέσματα προκύπτει επίσης συσχέτιση μεταξύ ανοσοϊστοχημικών εντοπίσεων της MMP-9 και των υπολοίπων υπό διερεύνηση μορίων. Προέκυψαν επίσης ποικίλες συσχετίσεις μεταξύ συγκεκριμένων προτύπων έκφρασης (pattern) και προγνωστικών παραγόντων. Η έκφραση της MMP-9 στο κυτταρόπλασμα των καρκινικών κυττάρων σχετίστηκε θετικά με τη λεμφαδενική προσβολή, αλλά αρνητικά με το μέγεθος του όγκου. Επίσης, η έκφραση του CXCR4 και της SDF-1 στα καρκινικά κύτταρα σχετίστηκε με την παρουσία οστικών μεταστάσεων και με τον ιστολογικό βαθμό κακοήθειας, αντίστοιχα. Επιπλέον, η ανοσοεντόπιση της SDF-1 στους ινοβλάστες του καρκινικού στρώματος συσχετίστηκε θετικά με την έκφραση του Ki67 και με το στάδιο κατά ΤΝΜ, ενώ η ανοσοεντόπιση της SDF-1 στα ενδοθηλιακά κύτταρα του καρκινικού στρώματος με την έκφραση του Her2. Η ανοσοϊστοχημική έκφραση του HIF-1α συσχετίστηκε αρνητικά με την έκφραση των στεροειδικών υποδοχέων ER και PR. Επιπλέον, η έκφραση της MMP-9 στους ινοβλάστες του καρκινικού στρώματος και η έκφραση της SDF-1 στα επιθηλιακά κύτταρα και στους ινοβλάστες του παρακείμενου μη καρκινικού ιστού συσχετίστηκαν με δυσμενέστερη επιβίωση. Το εύρημα αυτό τονίζει τη σημαντικότητα τόσο του στρώματος όσο και του ξενιστή στην παθογένεια του καρκίνου. Τα αποτελέσματα αυτά αναδεικνύουν τη σημαντικότητα των υπό μελέτη μορίων στην καρκινογένεση και στην εξέλιξη της νόσου. Για την επαλήθευση των αποτελεσμάτων αυτών απαιτείται η διενέργεια μελετών μεγαλύτερης κλίμακας ενώ προσεγγίσεις με λειτουργικές μεθοδολογίες θα μπορούσαν να αναδείξουν πιθανώς κοινά ή διαπλεκόμενα υποκείμενα μηνυματοδοτικά μονοπάτια στα οποία εμπλέκονται τα ως άνω μόρια.
Breast cancer is the most frequently diagnosed cancer in women. Despite the ongoing research in breast cancer tumorigenesis the underlying mechanisms are not yet well elucidated. In recent years, the interaction between tumour cells and tumour microenvironment has gained appreciation as an active participant in cancer pathophysiology. In the present study we…
Advisors/Committee Members: Παπαδάκη - Πέτρου, Ελένη, Papatheodorou, Haralabos, Παπαδάκη - Πέτρου, Ελένη, Δημόπουλος, Παναγιώτης, Καλόφωνος, Χαράλαμπος, Βαράκης, Ιωάννης, Σκόπα, Χρυσούλα, Παναγιωτάκης, Γεώργιος, Γυφτόπουλος, Κωνσταντίνος.
Subjects/Keywords: Ανοσοϊστοχημεία; Καρκίνος μαστού; Επιβίωση; Προγνωστικοί δείκτες; 616.994 490 75; Immunohistochemistry; Breast cancer; Survival; HIF-1; SDF-1; CXCR-4; MMP-9
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Παπαθεοδώρου, . (2011). Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CΧCR4) σε πρωτοπαθή καρκινώματα μαστού. (Doctoral Dissertation). University of Patras. Retrieved from http://hdl.handle.net/10889/5666
Chicago Manual of Style (16th Edition):
Παπαθεοδώρου, Χαράλαμπος. “Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CΧCR4) σε πρωτοπαθή καρκινώματα μαστού.” 2011. Doctoral Dissertation, University of Patras. Accessed March 07, 2021.
http://hdl.handle.net/10889/5666.
MLA Handbook (7th Edition):
Παπαθεοδώρου, Χαράλαμπος. “Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CΧCR4) σε πρωτοπαθή καρκινώματα μαστού.” 2011. Web. 07 Mar 2021.
Vancouver:
Παπαθεοδώρου . Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CΧCR4) σε πρωτοπαθή καρκινώματα μαστού. [Internet] [Doctoral dissertation]. University of Patras; 2011. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10889/5666.
Council of Science Editors:
Παπαθεοδώρου . Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CΧCR4) σε πρωτοπαθή καρκινώματα μαστού. [Doctoral Dissertation]. University of Patras; 2011. Available from: http://hdl.handle.net/10889/5666

Georgia Tech
13.
Duncanson, Stephanie.
Improving the bioartificial pancreas: Investigation of the effects of pro-survival and insulinotropic factor delivery and the development of PEGylated alginate microcapsules to support the function and survival of encapsulated islets and beta cells.
Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2014, Georgia Tech
URL: http://hdl.handle.net/1853/54015
► The development of a bioartificial pancreas (BAP) has the potential to substantially improve the treatment of insulin-dependent diabetes. Composed of insulin-secreting cells encapsulated in a…
(more)
▼ The development of a bioartificial pancreas (BAP) has the potential to substantially improve the treatment of insulin-dependent diabetes. Composed of insulin-secreting cells encapsulated in a hydrogel material, a BAP may provide superior glycemic regulation compared with conventional exogenous insulin-delivery therapies. Towards this goal, β- cells or islets encapsulated in alginate microcapsules remain a promising approach. Due to the limited supply of human islets, alternative cell sources are under investigation for incorporation into a BAP, including porcine islets and β- cell lines. Several challenges remain to clinical implementation, including loss of islet or β- cell function and viability following transplantation and host response to the transplanted microcapsules.
The objective of this work was to evaluate strategies to improve a BAP by supporting the function and survival of encapsulated islets and β -cells. Towards this goal, two areas were explored:
1) the provision of pro-survival and insulinotropic factors, namely, CXCL12 and GLP-
1 (or a GLP-
1 analog, Exendin-4), to encapsulated islets and β-cells and 2) modification of the alginate microcapsule to confer long-term resistance to host cell adhesion.
To achieve the first objective, methods to deliver both pro-survival and insulinotropic factors to a BAP were developed and their effects on encapsulated β-cells and porcine islets were studied, both in vitro and in vivo. Results demonstrate that delivery of pro-survival and insulinotropic factors is a promising strategy to prolong the survival and function of a BAP. To reduce host cell adhesion to the microcapsule, we employed covalent conjugation of PEG to the surface of alginate-PLL capsules to replace the un-crosslinked layer of alginate used in traditional alginate-PLL-alginate (APA) microcapsules. Results demonstrate that while PEGylation of alginate-PLL microcapsules initially reduced host cell adhesion over 2 weeks in vivo compared with APA capsules, the PEG coating did not provide long-term protection over 3 months. Taken together, these studies represent a multipronged approach towards improving the duration of BAP function, with the ultimate goal of advancing this technology to the clinic.
Advisors/Committee Members: Sambanis, Athanassios (advisor), Babensee, Julia (committee member), Champion, Julie (committee member), Temenoff, Johnna (committee member), Safley, Susan (committee member).
Subjects/Keywords: Bioartificial pancreas; Diabetes; Alginate microcapsule; Islet; Beta-cell; CXCL12; SDF-1; GLP-1; PEG; Hypoxia; Exendin-4
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Duncanson, S. (2014). Improving the bioartificial pancreas: Investigation of the effects of pro-survival and insulinotropic factor delivery and the development of PEGylated alginate microcapsules to support the function and survival of encapsulated islets and beta cells. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/54015
Chicago Manual of Style (16th Edition):
Duncanson, Stephanie. “Improving the bioartificial pancreas: Investigation of the effects of pro-survival and insulinotropic factor delivery and the development of PEGylated alginate microcapsules to support the function and survival of encapsulated islets and beta cells.” 2014. Doctoral Dissertation, Georgia Tech. Accessed March 07, 2021.
http://hdl.handle.net/1853/54015.
MLA Handbook (7th Edition):
Duncanson, Stephanie. “Improving the bioartificial pancreas: Investigation of the effects of pro-survival and insulinotropic factor delivery and the development of PEGylated alginate microcapsules to support the function and survival of encapsulated islets and beta cells.” 2014. Web. 07 Mar 2021.
Vancouver:
Duncanson S. Improving the bioartificial pancreas: Investigation of the effects of pro-survival and insulinotropic factor delivery and the development of PEGylated alginate microcapsules to support the function and survival of encapsulated islets and beta cells. [Internet] [Doctoral dissertation]. Georgia Tech; 2014. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1853/54015.
Council of Science Editors:
Duncanson S. Improving the bioartificial pancreas: Investigation of the effects of pro-survival and insulinotropic factor delivery and the development of PEGylated alginate microcapsules to support the function and survival of encapsulated islets and beta cells. [Doctoral Dissertation]. Georgia Tech; 2014. Available from: http://hdl.handle.net/1853/54015

University of Toronto
14.
Chen, Li-Hao (Henry).
Role of the SDF-1/CXCR4/eNOS Signaling Pathway in Chronic Kidney Disease.
Degree: 2012, University of Toronto
URL: http://hdl.handle.net/1807/33375
► Loss of the renal microvasculature is a common feature of almost all forms of chronic kidney disease (CKD). Here we explored the role of the…
(more)
▼ Loss of the renal microvasculature is a common feature of almost all forms of chronic kidney disease (CKD). Here we explored the role of the angiogenic chemokine stromal cell-derived factor-1-alpha (SDF-1) and its cognate receptor CXCR4 in experimental and human CKD. CXCR4 was present on endothelial cells and podocytes, while SDF-1 was detectable on podocytes, arteriolar smooth muscle cells, interstitial fibroblasts and occasional endothelial cells. CXCR4 mRNA was elevated in the kidneys of rats with CKD and chronic antagonism of CXCR4 accelerated renal decline and capillary loss. Acute SDF-1 infusion activated glomerular endothelial nitric oxide synthase (eNOS) in vivo, while functional response to SDF-1 was impaired in glomerular endothelial cells derived from eNOS-/- mice. Finally, CXCR4 mRNA was also found to be increased in biopsies of patients with secondary focal segmental glomerulosclerosis. These observations indicate that local eNOS-dependent SDF-1/CXCR4 signaling exerts a compensatory reno-protective effect in the setting of CKD.
MAST
Advisors/Committee Members: Advani, Andrew, Medical Science.
Subjects/Keywords: chronic kidney disease; SDF-1; CXCR4; eNOS; nephrology; focal and segmental glomerulosclerosis; 0306; 0307; 0379; 0566
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chen, L. (. (2012). Role of the SDF-1/CXCR4/eNOS Signaling Pathway in Chronic Kidney Disease. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/33375
Chicago Manual of Style (16th Edition):
Chen, Li-Hao (Henry). “Role of the SDF-1/CXCR4/eNOS Signaling Pathway in Chronic Kidney Disease.” 2012. Masters Thesis, University of Toronto. Accessed March 07, 2021.
http://hdl.handle.net/1807/33375.
MLA Handbook (7th Edition):
Chen, Li-Hao (Henry). “Role of the SDF-1/CXCR4/eNOS Signaling Pathway in Chronic Kidney Disease.” 2012. Web. 07 Mar 2021.
Vancouver:
Chen L(. Role of the SDF-1/CXCR4/eNOS Signaling Pathway in Chronic Kidney Disease. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1807/33375.
Council of Science Editors:
Chen L(. Role of the SDF-1/CXCR4/eNOS Signaling Pathway in Chronic Kidney Disease. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/33375

Virginia Commonwealth University
15.
Evans, Corey.
THE EFFECTS OF SDF-1α TREATMENT ON THE MIGRATION OF NEURAL STEM/PROGENITOR CELLS AFTER TRAUMATIC BRAIN INJURY.
Degree: MS, Anatomy & Neurobiology, 2011, Virginia Commonwealth University
URL: https://doi.org/10.25772/35SP-KP93
;
https://scholarscompass.vcu.edu/etd/2486
► Traumatic Brain Injury (TBI) is one of the leading causes of death and disability among young adults and has been a significant field in medical…
(more)
▼ Traumatic Brain Injury (TBI) is one of the leading causes of death and disability among young adults and has been a significant field in medical research over the past decades. Intensive studies focusing on how to repair tissue damage resulting from head injuries have discovered that the central nervous system (CNS) retains a regenerative capacity throughout life due to the persistent presence of neural stem/progenitor cells (NS/NPCs) in the neurogenic regions. In the normal brain, cells generated in the subventricular zone (SVZ) migrate along the rostral migratory stream (RMS) to the olfactory bulb and cells in the subgranular zone (SGZ) migrate laterally into the granule cell layer of the dentate gyrus. Directed movement of these NS/NPCs is controlled by a variety of factors, and among them the chemoattractant
SDF-1 is of particular importance. Studies have identified that the chemokine
SDF-1α and its receptor CXCR4 play an important role in guiding cell migration in many types of cells including NS/NPCs. The current study tested if
SDF-1 could be delivered through alginate to attract and guide migration of NS/NPCs and its progeny both in vitro and in vivo. Using a Boyden chamber migration assay, we found
SDF-1α either added directly in the medium or incorporated into alginate threads was capable of influencing migration of cultured NS/NPCs in a dose-dependent manner. In the in vivo study, when injected directly into the cerebral cortex,
SDF-
1 showed limited capability in inducing neuroblasts migration off the normal tract to the site of
SDF-1 injection. When
SDF-1 was delivered via alginate thread to the focal injury site at 2 days post TBI, significantly increased number of migrating neuroblasts derived from the SVZ was observed around the injury site. Increased expression of
SDF-1 receptor CXCR4 was observed in the NS/NPCs in the SVZ and around the injury site following TBI. These data suggest that bioactive
SDF-1α can be delivered via alginate thread and exogenous delivery of
SDF-1α and its interaction with receptor CXCR4 mediates migration of newly generated neurons from the SVZ to the site of injury following TBI. Collectively, our study indicates that
SDF-1α could be utilized as a guidance cue for tissue repair following brain injury.
Advisors/Committee Members: Dong Sun.
Subjects/Keywords: neural stem cells; SDF-1; TBI; CCI; stem cell migration; chemoattractant; Anatomy; Medicine and Health Sciences; Nervous System
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Evans, C. (2011). THE EFFECTS OF SDF-1α TREATMENT ON THE MIGRATION OF NEURAL STEM/PROGENITOR CELLS AFTER TRAUMATIC BRAIN INJURY. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/35SP-KP93 ; https://scholarscompass.vcu.edu/etd/2486
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Evans, Corey. “THE EFFECTS OF SDF-1α TREATMENT ON THE MIGRATION OF NEURAL STEM/PROGENITOR CELLS AFTER TRAUMATIC BRAIN INJURY.” 2011. Thesis, Virginia Commonwealth University. Accessed March 07, 2021.
https://doi.org/10.25772/35SP-KP93 ; https://scholarscompass.vcu.edu/etd/2486.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Evans, Corey. “THE EFFECTS OF SDF-1α TREATMENT ON THE MIGRATION OF NEURAL STEM/PROGENITOR CELLS AFTER TRAUMATIC BRAIN INJURY.” 2011. Web. 07 Mar 2021.
Vancouver:
Evans C. THE EFFECTS OF SDF-1α TREATMENT ON THE MIGRATION OF NEURAL STEM/PROGENITOR CELLS AFTER TRAUMATIC BRAIN INJURY. [Internet] [Thesis]. Virginia Commonwealth University; 2011. [cited 2021 Mar 07].
Available from: https://doi.org/10.25772/35SP-KP93 ; https://scholarscompass.vcu.edu/etd/2486.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Evans C. THE EFFECTS OF SDF-1α TREATMENT ON THE MIGRATION OF NEURAL STEM/PROGENITOR CELLS AFTER TRAUMATIC BRAIN INJURY. [Thesis]. Virginia Commonwealth University; 2011. Available from: https://doi.org/10.25772/35SP-KP93 ; https://scholarscompass.vcu.edu/etd/2486
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
16.
Vial, Ximena.
Design of Endothelial Progenitor Cellular Constructs for Therapeutic Angiogenesis Applications.
Degree: PhD, Biomedical Engineering (Engineering), 2013, University of Miami
URL: https://scholarlyrepository.miami.edu/oa_dissertations/1146
► The goal of therapeutic angiogenesis is the development of functional and mature vasculature by combining biological and physical cues that mimic the native extracellular matrix.…
(more)
▼ The goal of therapeutic angiogenesis is the development of functional and mature vasculature by combining biological and physical cues that mimic the native extracellular matrix. In this study we evaluated if immobilizing vascular endothelial growth factor (VEGF) gradients and
SDF-1α on gelatin nanofibrous scaffolds with different fiber orientations (i.e. random or aligned) influence the angiogenic potential of endothelial progenitor cells (EPCs) and human umbilical vein endothelial cells (HUVECs). Both cell types successfully adhered onto gelatin B scaffolds. VEGF gradients alone or combined with
SDF-1α as well as fiber orientation had a pronounced effect on cell behavior, morphology and orientation. Cells organized themselves parallel to the fibers of the electrospun scaffolds with the aligned orientation and developed a spindle-like morphology. Conversely, cells cultured on scaffolds with random fiber orientation, did not display directionality and appeared to have a rounder shape. Cell migration and capillary formation were found to be dependent on VEGF gradients,
SDF-1α presentation and cell type. These findings indicate that electrospun scaffolds are capable of regulating spatial growth factor presentation and influence cellular organization.
Advisors/Committee Members: Fotios M. Andreopoulos, Edward Dauer, Roberto Vazquez-Padron, Herman Cheung, Si Pham.
Subjects/Keywords: Angiogenesis; Electrospinning; HUVECs; EPCs; VEGF; SDF-1
…VEGF
bFGF
SDF-1
VEGF
VEGF
bFGF
TGF-β
HGF
VEGF
bFGF
VEGF
Collagen
Gelatin
Alginate
PLGA/PEG… …77
Figure 4.2: EPC response to the co-administration of VEGF gradients and SDF-1α
(… …SDF-1α… …and SDF-1α… …gradients and SDF-1α…
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Vial, X. (2013). Design of Endothelial Progenitor Cellular Constructs for Therapeutic Angiogenesis Applications. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1146
Chicago Manual of Style (16th Edition):
Vial, Ximena. “Design of Endothelial Progenitor Cellular Constructs for Therapeutic Angiogenesis Applications.” 2013. Doctoral Dissertation, University of Miami. Accessed March 07, 2021.
https://scholarlyrepository.miami.edu/oa_dissertations/1146.
MLA Handbook (7th Edition):
Vial, Ximena. “Design of Endothelial Progenitor Cellular Constructs for Therapeutic Angiogenesis Applications.” 2013. Web. 07 Mar 2021.
Vancouver:
Vial X. Design of Endothelial Progenitor Cellular Constructs for Therapeutic Angiogenesis Applications. [Internet] [Doctoral dissertation]. University of Miami; 2013. [cited 2021 Mar 07].
Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1146.
Council of Science Editors:
Vial X. Design of Endothelial Progenitor Cellular Constructs for Therapeutic Angiogenesis Applications. [Doctoral Dissertation]. University of Miami; 2013. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1146

Freie Universität Berlin
17.
Kränkel, Nicolle.
Veränderungen in der Kommunikation zwischen dem Endothel und myeloiden Zellen
bei Patienten mit kardiovaskulären Erkrankungen beeinflussen die vaskuläre
Verletzungsantwort.
Degree: 2018, Freie Universität Berlin
URL: https://refubium.fu-berlin.de/handle/fub188/13968
► Kardiovaskuläre Erkrankungen stellen aktuell die größte Gruppe nichtübertragbarer Erkrankungen weltweit. Einhergehend mit der weltweiten Änderung des Lebensstils – erhöhte Kalorienaufnahme, verringerte körperliche Aktivität, erhöhte Belastung…
(more)
▼ Kardiovaskuläre Erkrankungen stellen aktuell die größte Gruppe
nichtübertragbarer Erkrankungen weltweit. Einhergehend mit der weltweiten
Änderung des Lebensstils – erhöhte Kalorienaufnahme, verringerte körperliche
Aktivität, erhöhte Belastung der Umwelt mit Substanzen und Partikeln, die
inflammatorische Reaktionen auslösen und somit chronisch einen Stress auf das
Endothel ausüben – werden immer größere Anstrengungen notwendig sein, um die
Prävention und Behandlung kardiovaskulärer Erkrankungen zu stärken. Dies
erfordert die Zusammenarbeit von Wissenschaftlern und Klinikern auf
grundlagenwissenschaftlicher, prä-klinischer und klinischer Ebene, sowie einen
engen Bezug zu den Patientenpopulationen. Einschränkungen in der Funktion der
Endothelzellen sind grundlegend mit der Initiation und dem Fortschreiten
kardiovaskulärer Erkrankungen verbunden. Die Endothelfunktion selbst wird
durch verschiedene gewebsständige und zirkulierende Zellen mit parakriner
Funktion beeinflusst, was entweder funktionsunterstützend und erhaltend
wirken, oder im Gegensatz dazu den Verlust der Endothelfunktion noch
beschleunigen kann. Myeloide Zellen mit parakriner Funktion werden bei
Gefäßverletzungen oder bei Ischämie aus dem umliegenden Gewebe und aus der
Zirkulation rekrutiert und besitzen eine große funktionelle und
immunphänotypische Flexibilität. Die vorliegende Arbeit beschäftigt sich mit
Veränderungen der Interaktion zwischen parakrin wirkenden, myeloiden Zellen
und den Gefäßendothel bei Patienten mit kardiovaskulären Erkrankungen und mit
der Rekrutierung bestimmter Leukozytensubtypen an und in die geschädigte
Gefäßwand. Es wurden ex vivo-Assays entwickelt und optimiert, welche die
phänotypische und funktionelle Charakterisierung zirkulierender
Zellpopulationen aus Patienten und gesunden Kontrollprobanden ermöglichen.
Zudem wurde die Rekrutierung verscheidener Typen zirkulierender Zellen in
ischämisches Gewebe und an die verletzte Gefäßwand untersucht, sowie deren
molekulare Mediatoren charakterisiert. Ein Fokus der Arbeiten lag hierbei auf
dem Kinin-System und dem
SDF-
1/CXCR4 Signalweg. In beiden Fällen sind Pharmaka
verfügbar, die die Degradation der Mediatoren durch Angiotensin-converting
Enzyme und Dipeptidylpeptidase 4 hemmen können. Die Daten unterstützen das
Konzept, dass die Modulation der Funktion und der selektiven Rekrutierung
myeloider Zellen die Fähigkeit des Endothels unterstützt, die Kappilarisierung
und vaskuläre Reparaturprozesse zu initiieren. Weiterhin unterstreichen die
Daten die große Bedeutung myeloider Zellen für die Aufrechterhaltung der
Funktion der Blutgefäße. Einschränkungen der Kinin- und
SDF-
1-vermittelten
Funktionen bei myeloiden Zellen von Patienten sind daher eng mit
Funktionseinschränkungen des Endothels bei Patienten mit kardiovaskulären
Erkrankungen verbunden. Weiterführende Studien untersuchen die molekularen
Mechanismen der mikrovesikel-basierten Kommunikation zweischen Zelltypen,
besonders zwischen myeloiden Zellen und dem Gefäßendothel. Diese
Untersuchungen sollen zum Einen die Genauigkeit der…
Advisors/Committee Members: w (gender), Prof. Dr. med. Ulrich Laufs (firstReferee), Prof. Dr. med. Renate Schnabel (furtherReferee).
Subjects/Keywords: cardiovascular disease; response to injury; endothelium; myeloid cells; kinins; SDF-1; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kränkel, N. (2018). Veränderungen in der Kommunikation zwischen dem Endothel und myeloiden Zellen
bei Patienten mit kardiovaskulären Erkrankungen beeinflussen die vaskuläre
Verletzungsantwort. (Thesis). Freie Universität Berlin. Retrieved from https://refubium.fu-berlin.de/handle/fub188/13968
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kränkel, Nicolle. “Veränderungen in der Kommunikation zwischen dem Endothel und myeloiden Zellen
bei Patienten mit kardiovaskulären Erkrankungen beeinflussen die vaskuläre
Verletzungsantwort.” 2018. Thesis, Freie Universität Berlin. Accessed March 07, 2021.
https://refubium.fu-berlin.de/handle/fub188/13968.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kränkel, Nicolle. “Veränderungen in der Kommunikation zwischen dem Endothel und myeloiden Zellen
bei Patienten mit kardiovaskulären Erkrankungen beeinflussen die vaskuläre
Verletzungsantwort.” 2018. Web. 07 Mar 2021.
Vancouver:
Kränkel N. Veränderungen in der Kommunikation zwischen dem Endothel und myeloiden Zellen
bei Patienten mit kardiovaskulären Erkrankungen beeinflussen die vaskuläre
Verletzungsantwort. [Internet] [Thesis]. Freie Universität Berlin; 2018. [cited 2021 Mar 07].
Available from: https://refubium.fu-berlin.de/handle/fub188/13968.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kränkel N. Veränderungen in der Kommunikation zwischen dem Endothel und myeloiden Zellen
bei Patienten mit kardiovaskulären Erkrankungen beeinflussen die vaskuläre
Verletzungsantwort. [Thesis]. Freie Universität Berlin; 2018. Available from: https://refubium.fu-berlin.de/handle/fub188/13968
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
18.
Παπαθεοδώρου, Χαράλαμπος.
Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CXCR4) σε πρωτοπαθή καρκινώματα μαστού.
Degree: 2011, University of Patras; Πανεπιστήμιο Πατρών
URL: http://hdl.handle.net/10442/hedi/27005
► Breast cancer is the most frequently diagnosed cancer in women. Despite the ongoing research in breast cancer tumorigenesis the underlying mechanisms are not yet well…
(more)
▼ Breast cancer is the most frequently diagnosed cancer in women. Despite the ongoing research in breast cancer tumorigenesis the underlying mechanisms are not yet well elucidated. In recent years, the interaction between tumour cells and tumour microenvironment has gained appreciation as an active participant in cancer pathophysiology. In the present study we attempt to investigate the immunohistochemical staining of CXCR4, SDF-1, MMP-9 and HIF-1a in invasive breast cancer and adjacent normal breast tissue (including epithelial and stromal components) and to determine the relationship between different expression patterns and various tumor clinicopathological parameters and survival. The understudy molecules where chosen due to their crucial role in different steps of breast cancer progression (tumor growth, hypoxia, neovascularisation, invasiveness etc.). All molecules showed statistically significant higher expression in cancer tissue compared to expression in the adjacent noncancerous tissue. Our results reveal a correlation between expression patterns of MMP-9 and the other understudy molecules (SDF1, CXCR4 and HIF-1a). Furthermore, MMP-9 expression in fibroblasts of cancer stroma and SDF-1 expression in normal epithelial cells and fibroblasts of adjacent normal stroma were associated with poorer survival, underscoring the importance of tumor microenvironment and host derived molecules in tumor progression. There were also various correlations between specific expression patterns and prognostic factors: MMP-9 expression in cancer cells was positively correlated with lymph node involvement, but negatively with tumor size, while CXCR4 and SDF-1 expression in cancer cells was positively correlated with bone metastases and tumor grade, respectively. Furthermore, SDF-1 immunoexpression of cancer stromal fibroblasts was positively correlated with Ki67 expression and TNM stage, whereas SDF-1 immunoexpression in endothelial cells of cancer stroma was positively correlated with Her2 expression. HIF-1a expression in cancer cells was negatively correlated with expression of steroid receptors. The abovementioned results underline the importance of the understudy molecules in carcinogenesis and tumor progression. Larger scale studies are necessary to confirm our results, while functional approaches could possibly reveal common or interwoven molecular pathways for the understudy molecules.
Ο καρκίνος του μαστού αποτελεί τον πιο συχνό τύπο καρκίνου των γυναικών. Παρότι η σχετική έρευνα είναι αρκετά εκτεταμένη, οι υποκείμενοι μηχανισμοί δεν έχουν πλήρως αποσαφηνιστεί. Πρόσφατες μελέτες έχουν αναδείξει τη σημαντικότητα της διαντίδρασης των καρκινικών κυττάρων και του καρκινικού μικροπεριβάλλοντος ως μια κομβική συνιστώσα στη παθοφυσιολογία της νόσου. Σκοπός της παρούσας μελέτης είναι η διερεύνηση της ανοσοϊστοχημικής έκφρασης του υποδοχέα CXCR4, της χημοκίνης SDF-1, της μεταλλοπρωτεϊνάσης ΜΜΡ-9 και του παράγοντα HIF-1a σε διηθητικά καρκινώματα του μαστού και στον παρακείμενο μη καρκινικό ιστό (τόσο στο επιθηλιακό όσο και στο…
Subjects/Keywords: Καρκίνος μαστού; Ανοσοϊστοχημεία; Προγνωστικοί δείκτες; Επιβίωση; SDF-1; CXCR4; MMP-9; HIF-1a; Breast cancer; Immunohistochemistry (IHC)
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Παπαθεοδώρου, . . (2011). Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CXCR4) σε πρωτοπαθή καρκινώματα μαστού. (Thesis). University of Patras; Πανεπιστήμιο Πατρών. Retrieved from http://hdl.handle.net/10442/hedi/27005
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Παπαθεοδώρου, Χαράλαμπος. “Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CXCR4) σε πρωτοπαθή καρκινώματα μαστού.” 2011. Thesis, University of Patras; Πανεπιστήμιο Πατρών. Accessed March 07, 2021.
http://hdl.handle.net/10442/hedi/27005.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Παπαθεοδώρου, Χαράλαμπος. “Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CXCR4) σε πρωτοπαθή καρκινώματα μαστού.” 2011. Web. 07 Mar 2021.
Vancouver:
Παπαθεοδώρου . Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CXCR4) σε πρωτοπαθή καρκινώματα μαστού. [Internet] [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2011. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10442/hedi/27005.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Παπαθεοδώρου . Προγνωστική αξία ανοσοϊστοχημικών μοριακών δεικτών (άξονας SDF1 / CXCR4) σε πρωτοπαθή καρκινώματα μαστού. [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2011. Available from: http://hdl.handle.net/10442/hedi/27005
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
19.
Kontogianni, Panagiota.
Ανίχνευση των γενετικών πολυμορφισμών της κασπάσης-9, του προερχόμενου από το στρωματικό κύτταρο παράγοντα-1 και της Ε-σελεκτίνης στον καρκίνο του μαστού.
Degree: 2014, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)
URL: http://hdl.handle.net/10442/hedi/40608
► Caspases (CASPs), play a crucial role in the development and progression of cancer. We evaluated the association between two polymorphisms (rs4645978 and rs4645981) of the…
(more)
▼ Caspases (CASPs), play a crucial role in the development and progression of cancer. We evaluated the association between two polymorphisms (rs4645978 and rs4645981) of the CASP9 gene and the risk of breast cancer (BC). Genotypes and allelic frequencies for the two polymorphisms were determined in 261 patients with breast cancer and 480 healthy controls. Polymerase chain reaction-restriction fragment length polymorphisms were used, and statistical significance was determined by the χ2 test. Carriers of the rs4645978 G allele (AG and GG genotypes) were at higher risk for BC than individuals with other genotypes (odds ratio (OR) 1.59, 95% confidence interval (CI) 1.07-2.37, p =0.022). The rs4645978 GG genotype, in particular, was associated with the highest risk for BC development (OR 2.25, 95% CI 1.45-3.49, p=0.0003). Similarly, individuals with at least one rs4645981 T allele were at a significantly increased risk of developing BC compared with those harboring the CC genotype (OR 2.75, 95% CI 1.99-3.78, p<0.0001), and the risk of BC increased with increasing numbers of rs4645981 T alleles (OR 2.66, 95% CI 1.91-3.69, p<0.0001 for the CT genotype; OR 3.95, 95% CI 1.58-9.88, p=0.004 for the TT genotype). The CASP9 promoter polymorphisms rs4645978 and rs4645981 are associated with BC susceptibility and suggest that CASP9 transcriptional regulation is an important factor during BC development. Breast cancer is prone to metastasis even in early stage disease. Stromal cell-derived factor-1 (SDF-1) is a chemokine that has been associated with the egress of cancer cells from the primary focus and homing to distant sites, while E-selectin has been implicated in their transendothelial migration. This study was performed to evaluate the association between SDF-1–3’ A and E-selectin S128R—two polymorphisms associated with enhanced function—and the risk of breast cancer, as well as their influence on breast cancer outcome. The frequencies for the wild-type (GG), GA and AA genotypes of SDF-1 were 43.7, 45.2, and 11.1 % in patients, and 51.5, 41.3, and 7.3 % in healthy controls, respectively, while the SDF-1–3’ A allelic frequency was 33.7 % at patients and 27.9 % at controls. The SDF-1–3’ A carrier group of patients and the A allele of SDF-1 were overrepresented among the breast cancer cases (p = 0.04 and 0.02, respectively). For the E-selectin S128R polymorphism, the frequencies for the wild-type (AA), AC and CC genotypes were 58.6, 38.3, and 3.1 % in patients and 63.8, 31.4, and 3.8 % in controls, respectively, while the C allelic frequency was 22.2 % for patients and 19.5 % for controls. The CC genotype was associated with poorer survival. Otherwise, no significant association was detected between examined genotypes and tumor characteristics. Overall, our findings support that the SDF-1–3’ A confers increased susceptibility to breast cancer and that the E-selectin S128R CC genotype may be related to poorer prognosis. Investigation in bigger cohorts of patients is warranted.
Οι κασπάσες παίζουν έναν κρίσιμο ρόλο στην ανάπτυξη…
Subjects/Keywords: Καρκίνος μαστού; Κασπάση-9; Ε-σελεκτίνη; Πολυμορφισμοί; Breast cancer; Caspase-9; SDF-1; E-selectin; Polymorphisms
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kontogianni, P. (2014). Ανίχνευση των γενετικών πολυμορφισμών της κασπάσης-9, του προερχόμενου από το στρωματικό κύτταρο παράγοντα-1 και της Ε-σελεκτίνης στον καρκίνο του μαστού. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/40608
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kontogianni, Panagiota. “Ανίχνευση των γενετικών πολυμορφισμών της κασπάσης-9, του προερχόμενου από το στρωματικό κύτταρο παράγοντα-1 και της Ε-σελεκτίνης στον καρκίνο του μαστού.” 2014. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed March 07, 2021.
http://hdl.handle.net/10442/hedi/40608.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kontogianni, Panagiota. “Ανίχνευση των γενετικών πολυμορφισμών της κασπάσης-9, του προερχόμενου από το στρωματικό κύτταρο παράγοντα-1 και της Ε-σελεκτίνης στον καρκίνο του μαστού.” 2014. Web. 07 Mar 2021.
Vancouver:
Kontogianni P. Ανίχνευση των γενετικών πολυμορφισμών της κασπάσης-9, του προερχόμενου από το στρωματικό κύτταρο παράγοντα-1 και της Ε-σελεκτίνης στον καρκίνο του μαστού. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10442/hedi/40608.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kontogianni P. Ανίχνευση των γενετικών πολυμορφισμών της κασπάσης-9, του προερχόμενου από το στρωματικό κύτταρο παράγοντα-1 και της Ε-σελεκτίνης στον καρκίνο του μαστού. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. Available from: http://hdl.handle.net/10442/hedi/40608
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas – Austin
20.
Rybalko, Viktoriya Yurievna.
The development of immunomodulatory approaches to restore skeletal muscle function after injury.
Degree: PhD, Kinesiology, 2015, University of Texas – Austin
URL: http://hdl.handle.net/2152/31473
► Efficient restoration of skeletal muscle function after severe injury is a major goal of intervention therapies. Ischemia/reperfusion (I/R) injury to skeletal muscle leads to exaggerated…
(more)
▼ Efficient restoration of skeletal muscle function after severe injury is a major goal of intervention therapies. Ischemia/reperfusion (I/R) injury to skeletal muscle leads to exaggerated inflammatory response and significant ultrastructural tissue damage slowing restoration of muscular structure and function. Herein, we used animal model of tourniquet-induced ischemia/reperfusion injury (TK-I/R) to test the effects of exogenously delivered growth factors and cells on skeletal muscle regeneration. The delivery of PEGylated fibrin along with stromal cell derived factor-1α and/or insulin-like growth factor-I into acutely injured muscle, differentially affected functional muscle regeneration. These data suggest that local balance and release kinetics of growth factors in the tissue microenvironment can significantly impact the success of skeletal muscle repair. Cell-mediated treatment of I/R-injured muscle demonstrated significant tissue regeneration using adoptively transferred and in vitro polarized macrophages. Functional activation status of transplanted macrophage populations impacted the outcome of muscle repair. We showed that increasing macrophage populations at the site of injury in temporally regulated manner is beneficial for efficient recovery of muscle force and function.
Advisors/Committee Members: Farrar, Roger P. (advisor), Suggs, Laura J (committee member), Brothers, Robert M (committee member), Thompson, Wesley J (committee member), Adamo, Martin L (committee member).
Subjects/Keywords: Pegylated fibrin; Direct transfer; Biodegradable gel; Macrophages; Muscle; Regeneration; Cell-mediated; IGF-I; SDF-1; Functional recovery
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Rybalko, V. Y. (2015). The development of immunomodulatory approaches to restore skeletal muscle function after injury. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/31473
Chicago Manual of Style (16th Edition):
Rybalko, Viktoriya Yurievna. “The development of immunomodulatory approaches to restore skeletal muscle function after injury.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed March 07, 2021.
http://hdl.handle.net/2152/31473.
MLA Handbook (7th Edition):
Rybalko, Viktoriya Yurievna. “The development of immunomodulatory approaches to restore skeletal muscle function after injury.” 2015. Web. 07 Mar 2021.
Vancouver:
Rybalko VY. The development of immunomodulatory approaches to restore skeletal muscle function after injury. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152/31473.
Council of Science Editors:
Rybalko VY. The development of immunomodulatory approaches to restore skeletal muscle function after injury. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/31473
21.
Machado, Isabel Daufenback.
Mecanismos moleculares da ação dos glicocorticóides endógenos e da anexina-A1 sobre o tráfego de neutrófilos: caracterização da ação sobre os eixos SDF-1α/CXCR4 e IL-17/IL-23/G-CSF.
Degree: PhD, Análises Clínicas, 2013, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-27022014-105135/
;
► O tráfego de leucócitos é um processo complexo, dependente da ação de inúmeras substâncias químicas, além da perfeita interação celular. Desta forma, este estudo teve…
(more)
▼ O tráfego de leucócitos é um processo complexo, dependente da ação de inúmeras substâncias químicas, além da perfeita interação celular. Desta forma, este estudo teve como objetivo avaliar a ação dos GCe e da ANXA1 sobre o eixo
SDF-
1α/CXCR4 e IL-17/IL-23/G-CSF e sobre a expressão de moléculas de adesão CD18, CD49d e CD62L. Foram utilizados camundongos machos Balb/C selvagens (WT) ou ANXA1-/-. As avaliações foram realizadas em condições basais, na presença de altas concentrações de GCe e na vigência de processo inflamatório, induzidos pela administração de ACTH (5 µg/animal, i.p.) ou pela injeção de LPS (100 µg/kg, i.p.), respectivamente, ou na ausência da ação dos GCe, pela ação do RU 38486 (RU, 10 mg/kg, i.p.). A participação da ANXA1 e do receptor FPR2 foi avaliada pelo pré-tratamento com Ac2-26 (
1 mg/Kg, i.p.) ou com BOC2 (10 µg/animal, i.p.) durante 4 dias,
1 vez ao dia. A quantificação total e diferencial das células foi realizada em câmara de Neubauer e em esfregaços corados por May-Grunwald ou citometria de fluxo. As quantificações de CXCR2, CXCR4, FPR2, CD18, CD49d, CD62L e maturação granulocítica (CD11b/Ly6G) em células da medula e da circulação foram realizadas por citometria de fluxo. A expressão de ANXA1 nos tecidos do estomago e do baço foi realizada por western blotting e nas células da medula óssea e sangue circulante foi realizada por imunofluorescência. As quantificações de IL-17, IL-23, G-CSF,
SDF-
1α e corticosterona foram realizadas por ELISA. A quimiotaxia de neutrófilos da medula óssea e sangue periférico foi ensaiada na placa de quimiotaxia com filtro de poro de 8 µm. A fagocitose de neutrófilos apoptóticos por macrófagos da medula óssea foi avaliada por ensaio in vitro. Para verificar os efeitos do ACTH na migração de neutrófilos no processo inflamatório, foi empregado o modelo de bolsa de ar (100 µg/mL; LPS); e o comportamento dos leucócitos circulantes de animais tratados com ACTH foi avaliado pela técnica de microscopia intravital. Os resultados obtidos, que estão apresentados em quatro temáticas, mostraram que:
1) neutrófilos da medula óssea e sangue periférico expressam ANXA1 no citoplasma e membrana, bem como o receptor FPR2, constitutivamente, e a expressão de ambos é regulada pelos GCe. A ANXA1, via receptor FPR2 expresso em células da medula óssea, controlam a maturação neutrofílica e o tráfego destas células da medula óssea para o sangue. A ANXA1, via interação ao FPR2, controla o clearance de neutrófilos do sangue para a medula óssea, modulando o eixo
SDF-
1α/CXCR4; 2) A administração do ACTH causa neutrofilia e os neutrófilos circulantes são ANXA1+, CD18+, CD49d+, CD62L+, mostrando que injeção do ACTH in vivo altera o fenótipo destas células na circulação. Estas modificações alteram o comportamento dos neutrófilos na circulação, bem como a migração para a bolsa de ar na vigência de inflamação e para os tecidos de clearance. Estes efeitos podem ser dependentes, pelo menos em parte, da inibição de migração orientada, já que quimiotaxia frente ao…
Advisors/Committee Members: Farsky, Sandra Helena Poliselli.
Subjects/Keywords: ACTH; ACTH; Adhesion molecules; Anexina-A1; Annexin-A1; Endogenous glucocorticoids; Glicocorticóides endógenos; IL-17/IL-23/G-CSF; IL-17/IL-23/G-CSF axis; Moléculas de adesão; Neutrófilo; Neutrophils; SDF-1α; /CXCR4; SDF-1α; /CXCR4 axis
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Machado, I. D. (2013). Mecanismos moleculares da ação dos glicocorticóides endógenos e da anexina-A1 sobre o tráfego de neutrófilos: caracterização da ação sobre os eixos SDF-1α/CXCR4 e IL-17/IL-23/G-CSF. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/9/9136/tde-27022014-105135/ ;
Chicago Manual of Style (16th Edition):
Machado, Isabel Daufenback. “Mecanismos moleculares da ação dos glicocorticóides endógenos e da anexina-A1 sobre o tráfego de neutrófilos: caracterização da ação sobre os eixos SDF-1α/CXCR4 e IL-17/IL-23/G-CSF.” 2013. Doctoral Dissertation, University of São Paulo. Accessed March 07, 2021.
http://www.teses.usp.br/teses/disponiveis/9/9136/tde-27022014-105135/ ;.
MLA Handbook (7th Edition):
Machado, Isabel Daufenback. “Mecanismos moleculares da ação dos glicocorticóides endógenos e da anexina-A1 sobre o tráfego de neutrófilos: caracterização da ação sobre os eixos SDF-1α/CXCR4 e IL-17/IL-23/G-CSF.” 2013. Web. 07 Mar 2021.
Vancouver:
Machado ID. Mecanismos moleculares da ação dos glicocorticóides endógenos e da anexina-A1 sobre o tráfego de neutrófilos: caracterização da ação sobre os eixos SDF-1α/CXCR4 e IL-17/IL-23/G-CSF. [Internet] [Doctoral dissertation]. University of São Paulo; 2013. [cited 2021 Mar 07].
Available from: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-27022014-105135/ ;.
Council of Science Editors:
Machado ID. Mecanismos moleculares da ação dos glicocorticóides endógenos e da anexina-A1 sobre o tráfego de neutrófilos: caracterização da ação sobre os eixos SDF-1α/CXCR4 e IL-17/IL-23/G-CSF. [Doctoral Dissertation]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-27022014-105135/ ;

Queens University
22.
Virani, Sophia.
Role of Stromal Cell-Derived Factor-1 in Neoangiogenesis in Endometriosis Lesions
.
Degree: Anatomy and Cell Biology, 2011, Queens University
URL: http://hdl.handle.net/1974/6920
► Endometriosis affects 5-10% of women and is characterized by the growth of endometrial tissue outside of the uterus. Treatment for endometriosis primarily focuses on symptom…
(more)
▼ Endometriosis affects 5-10% of women and is characterized by the growth of endometrial tissue outside of the uterus. Treatment for endometriosis primarily focuses on symptom relief, is short term with severe side effects and often leads to recurrence of the condition. Establishing new blood supply is a fundamental requirement for endometriosis lesions growth. This has led to the idea that antiangiogenic therapy may be a successful approach for inhibiting endometriosis. Recent evidence indicates that endothelial progenitor cells (EPCs) contribute to neoangiogenesis of endometriotic lesions. These EPCs are recruited to the lesion site by stromal cell-derived factor-1 (SDF-1). We hypothesize that SDF-1 is central to the neoangiogenesis and survival of endometriotic lesions and that administration of SDF-1 blocking antibody will inhibit lesion growth by inhibiting angiogenesis in a murine model of endometriosis. Immunohistochemistry for SDF-1 and CD34 was performed on human endometriosis and normal endometrial samples. Quantification of SDF-1 and EPCs was performed in the blood of endometriosis patients and controls using ELISA and flow cytometry, respectively. A new mouse model of endometriosis was developed using BALB/c-Rag2-/-/IL2rg-/- mice to investigate role of SDF-1 in neoangiogenesis. Either SDF-1 blocking antibody or an isotype control was administered on a weekly basis for four weeks. Weekly samples of peripheral blood from mice were analyzed for SDF-1, other cytokines of interest and EPCs. Mice were euthanized at seven weeks to observe lesion growth and blood vessel development. Our results indicate overabundance of SDF-1 and CD34+ progenitor cells in human endometriotic lesions compared to eutopic endometrium. In the mouse model, SDF-1 and circulating EPC levels decreased from pre-treatment levels after one week, and remained constant over the course of the treatment in both SDF-1 blocking antibody and isotype control groups. In the SDF-1 blocking group, reduced vascularity of lesions, identified by immunofluorescence staining for CD31, was revealed compared to isotype controls. These findings suggest that SDF-1 may be responsible for CD34+ progenitor cell recruitment to the neoangiogenic sites in endometriosis. Blocking of SDF-1 reduces neovascularization of human endometriotic lesions in a mouse model. Further studies on blocking SDF-1 in combination with other antiangiogenic agents are needed.
Subjects/Keywords: Endothelial progenitor cells
;
EPCs
;
Endometriosis
;
Sndometrium
;
Mouse Model of Endometriosis
;
Stromal Cell-Derived Factor-1
;
cEPCs
;
Circulating Endothelial Progenitor Cells
;
SDF-1
;
Angiogenesis
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Virani, S. (2011). Role of Stromal Cell-Derived Factor-1 in Neoangiogenesis in Endometriosis Lesions
. (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/6920
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Virani, Sophia. “Role of Stromal Cell-Derived Factor-1 in Neoangiogenesis in Endometriosis Lesions
.” 2011. Thesis, Queens University. Accessed March 07, 2021.
http://hdl.handle.net/1974/6920.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Virani, Sophia. “Role of Stromal Cell-Derived Factor-1 in Neoangiogenesis in Endometriosis Lesions
.” 2011. Web. 07 Mar 2021.
Vancouver:
Virani S. Role of Stromal Cell-Derived Factor-1 in Neoangiogenesis in Endometriosis Lesions
. [Internet] [Thesis]. Queens University; 2011. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1974/6920.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Virani S. Role of Stromal Cell-Derived Factor-1 in Neoangiogenesis in Endometriosis Lesions
. [Thesis]. Queens University; 2011. Available from: http://hdl.handle.net/1974/6920
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
23.
Şahin, Erhan.
Resveratrol ile muamele edilmiş yağ dokusu kaynaklı mezenşimal kök hücre sitokinlerinin A549 kanser hücresine etkilerinin araştırılması
.
Degree: ESOGÜ, Tıp Fakültesi, Histoloji ve Embriyoloji, 2016, Eskisehir Osmangazi University
URL: http://hdl.handle.net/11684/391
► Günümüzde kök hücre tedavileri, tıbbın birçok alanında deneysel veya bazı alanlarında da klinik olarak kullanılan önemli tedavi yöntemlerindendir. Farklı tedavi yöntemleri kullanılmasına rağmen henüz kanseri…
(more)
▼ Günümüzde kök hücre tedavileri, tıbbın birçok alanında deneysel veya bazı alanlarında da klinik olarak kullanılan önemli tedavi yöntemlerindendir. Farklı tedavi yöntemleri kullanılmasına rağmen henüz kanseri eradike edebilecek bir tedavi mevcut değildir. Akciğer kanseri en sık görülen kanser türleri arasındadır. Birçok deneysel çalışmada tedavi edici ve koruyucu özelliği gösterilen MKH’nin kanser modellerinde kanserli hücreleri baskıladığı ve çoğalmalarını durdurduğu bildirilmiştir. Ancak son yıllarda kanser tedavisi için kök hücrelerin kullanıldığı çalışmalarda; kök hücrelerin kanser oluşumunu tetiklediği, kitleyi büyüttüğü, yeni damarların oluşumuna ve kanserin invazyonuna yardımcı olduğu gösterilmiştir. MKH’ler ile kanser hücreleri arasındaki iletişimin MKH’lerden salınan sitokinler yardımıyla sağlandığı bilinmektedir. MKH’nin salgıladığı bu sitokinlerin varlığı ve kanserli hücreler üzerindeki etkisi MKH’lerin tedavi güvenilirliğini azaltmaktadır. Resveratrolün inflamasyon, oksidatif stres, kanser oluşması ve ilerlemesi, platelet agregasyonu, aterosklerozis ve yaşlanma gibi birçok biyolojik aktivitede olumlu görev aldığı gösterilmiştir. Bu çalışmanın amacı, MKH’ler ile A549 akciğer kanser hücrelerini in-vitro olarak aynı ortamda tutarak, MKH’lerin kanserli hücreleri desteklerken kullandığı sitokinleri, faydalı ve anti kanserojenik özelliğiyle bilinen resveratrol ile baskılayarak, kanserin tedavisinde çok önemli yeri olan MKH’lerin kullanımını ve tedavinin güvenilirliğini araştırmaktır.
Bu çalışmada hücre kültürü seviyesinde 6 ayrı grup oluşturularak çalışılmıştır. MKH'lerden salınan sitokinler (IL 6, CCL5, VEGF,
SDF-
1) ve resveratrolün bu sitokinler üzerindeki etkileri toplanan medyumlarda ELISA, western blot ve gerçek zamanlı PCR (rt-PCR) yöntemleriyle araştırılmıştır. Deneyimizde in-vitro sitotoksisite testleri yapılmıştır. Fluoresan boyama ile morfolojik inceleme (DAPI boyama) yapılmıştır.
Yaptığımız sitotoksisite deneyleri sonucunda A549 kanser hücrelerinde ve MKH’de güvenli doz 1μM olarak bulunmuştur. DAPI floresan boyaması sonucunda resveratrolün ve MKH’nin A549 kanser hücresi üzerinde apoptotik etkisi görülmemiştir. ELISA ve western blot deneyi ile gruplar arası sitokin miktar değişimine baktığımızda IL-6 ve VEGF sitokinlerinin ifade olduğu,
SDF-
1 ve CCl-5 salınımının olmadığı tespit edilmiştir. Rt-PCR deneyleri ile VEGF mRNA ekspresyonuna bakılmış, ELISA ve western blot deneyleri ile paralellik gösterdiği bulunmuştur. Gruplar arası sitokin salınımına baktığımızda en yüksek IL-6 ve VEGF salınımının A549+MKH grubunda olduğu resveratrolün anlamlı bir şekilde bu salınımı azalttığı bulundu.
Sonuç olarak IL-6 ve VEGF salınımı A549 kanser hücreleri ve MKH’leri bir arada bulunduğunda artmaktadır. Resveratrol bu artışı anlamlı bir şekilde düşürmektedir. Tüm gruplarda
SDF-
1 ve CCL-5 salınımı gözlenmedi.
Advisors/Committee Members: Bayçu, Cengiz (advisor).
Subjects/Keywords: Mezenşimal Kök Hücre;
A549 Kanser Hücresi;
IL-6;
VEGF;
SDF-1;
CCL-5;
Resveratrol;
Mesenchymal Stem Cells;
VEGF and Resveratrol;
A549 Cancer Cells
Record Details
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Şahin, E. (2016). Resveratrol ile muamele edilmiş yağ dokusu kaynaklı mezenşimal kök hücre sitokinlerinin A549 kanser hücresine etkilerinin araştırılması
. (Thesis). Eskisehir Osmangazi University. Retrieved from http://hdl.handle.net/11684/391
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Şahin, Erhan. “Resveratrol ile muamele edilmiş yağ dokusu kaynaklı mezenşimal kök hücre sitokinlerinin A549 kanser hücresine etkilerinin araştırılması
.” 2016. Thesis, Eskisehir Osmangazi University. Accessed March 07, 2021.
http://hdl.handle.net/11684/391.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Şahin, Erhan. “Resveratrol ile muamele edilmiş yağ dokusu kaynaklı mezenşimal kök hücre sitokinlerinin A549 kanser hücresine etkilerinin araştırılması
.” 2016. Web. 07 Mar 2021.
Vancouver:
Şahin E. Resveratrol ile muamele edilmiş yağ dokusu kaynaklı mezenşimal kök hücre sitokinlerinin A549 kanser hücresine etkilerinin araştırılması
. [Internet] [Thesis]. Eskisehir Osmangazi University; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/11684/391.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Şahin E. Resveratrol ile muamele edilmiş yağ dokusu kaynaklı mezenşimal kök hücre sitokinlerinin A549 kanser hücresine etkilerinin araştırılması
. [Thesis]. Eskisehir Osmangazi University; 2016. Available from: http://hdl.handle.net/11684/391
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Michigan
24.
Li, Qin.
Functional analysis of chemokine signaling in zebrafish development.
Degree: PhD, Molecular biology, 2004, University of Michigan
URL: http://hdl.handle.net/2027.42/124484
► Chemokines are a large family of secreted proteins that are important to the migration of leukocytes during hematopoiesis and inflammation. Chemokines and their receptors are…
(more)
▼ Chemokines are a large family of secreted proteins that are important to the migration of leukocytes during hematopoiesis and inflammation. Chemokines and their receptors are also widely distributed in the nervous system. Although recent investigations are beginning to elucidate chemokine function within the nervous system, relatively little is known about the neuronal function of this important class of molecules. To better appreciate the function of chemokines, the role of signaling by
SDF-
1 through its CXCR4 receptor was analyzed in zebrafish embryos. The
SDF-
1/CXCR4b expression pattern suggested that
SDF-
1/CXCR4 signaling may guide retinal ganglion cell (RGC) axons within the retina to the optic stalk to exit the retina. Both misexpression of the ligand and antisense knockdown of the ligand and/or receptor decreased the number of differentiating RGCs. Furthermore, lower levels of knockdown and a genetic mutation of CXCR4 did not affect the normal complement of RGCs but did induce their axons to follow aberrant pathways within the retina. RGCs extend aberrant axons toward ectopic source
SDF-
1, suggesting
SDF-
1 is a chemoattractant for retinal axons. These data suggest that chemokine signaling is essential at multiple stages in the development of RGCs. The
SDF-1a/CXCR4b expression pattern also suggested that
SDF-
1/CXCR4 signaling was important for guiding migration by sensory cells known as the migrating primordium of the posterior lateral line. Ubiquitous induction of the ligand in transgenic embryos, antisense knockdown of the ligand or receptor, and a genetic receptor mutation all disrupted migration by the primordium. Furthermore, in embryos in which endogenous
SDF-
1 was knocked down, the primordium migrated towards exogenous sources of
SDF-
1. These data demonstrate that
SDF-
1 signaling mediated via CXCR4 functions as a chemoattractant for the migrating primordium and that chemokine signaling is both necessary and sufficient for directing primordium migration.
SDF-1b/CXCR4a expression also suggests that chemokine signaling might be involved in angiogenesis in zebrafish. Ubiquitous expression of
SDF-
1 led to circulation defects and cardiac edema. Antisense knockdown of either the ligand or the receptor caused defect in intersegmental vessel formation. Further experiments are necessary to elucidate the exact function of
SDF-
1/CXCR4 in blood vessel formation and/or remodeling.
Advisors/Committee Members: Kuwada, John Y. (advisor).
Subjects/Keywords: Analysis; Chemokine; Development; Functional; Nervous System; Retinal Ganglion Cells; Sdf-1; Signaling; Zebrafish
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Li, Q. (2004). Functional analysis of chemokine signaling in zebrafish development. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/124484
Chicago Manual of Style (16th Edition):
Li, Qin. “Functional analysis of chemokine signaling in zebrafish development.” 2004. Doctoral Dissertation, University of Michigan. Accessed March 07, 2021.
http://hdl.handle.net/2027.42/124484.
MLA Handbook (7th Edition):
Li, Qin. “Functional analysis of chemokine signaling in zebrafish development.” 2004. Web. 07 Mar 2021.
Vancouver:
Li Q. Functional analysis of chemokine signaling in zebrafish development. [Internet] [Doctoral dissertation]. University of Michigan; 2004. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2027.42/124484.
Council of Science Editors:
Li Q. Functional analysis of chemokine signaling in zebrafish development. [Doctoral Dissertation]. University of Michigan; 2004. Available from: http://hdl.handle.net/2027.42/124484

Universitat Pompeu Fabra
25.
Simonte, Giacoma, 1984-.
Endogenous mobilization of bone-marrow cells into murine retina induces fusion-mediated reprogramming of Müller glia cells.
Degree: Departament de Ciències Experimentals i de la Salut, 2016, Universitat Pompeu Fabra
URL: http://hdl.handle.net/10803/543845
► Mi proyecto de doctorado ha sido enfocado en entender si las células de la medula (BMCs) pueden participar en la reparación de la retina del…
(more)
▼ Mi proyecto de doctorado ha sido enfocado en entender si las células de la medula (BMCs) pueden participar en la reparación de la retina del ratón después de causar un daño con N-Methyl-D-aspartate (NMDA). Hemos querido explorar la posibilidad de que las BMCs pudiesen migrar desde la sangre periférica hasta la retina dañada y fusionarse con las neuronas retinianas.
Hemos encontrado que las células endógenas de la médula son movilizadas hacia la retina del ratón después de causar el referido daño fusionándose con las neuronas de la retina, principalmente con las células gliales Müller (MG).
Las células MG empiezan un proceso de desdiferenciación y reprogramación después de causar el daño de NMDA, y acaban diferenciándose en células ganglionares y amacrinas a través de un mecanismo de fusión celular. Este proceso neurogénico está influenciado también de la vía de señalación
SDF-/CXCR4, cuando hemos manipulado esta vía de señalación celular hemos sido capaces de aumentar o bloquear la capacidad de las células MG de reprogramarse y de generar nuevas neuronas.
En general hemos descrito un nuevo mecanismo mediante el cual las células MG pueden desdiferenciarse a través de un proceso de fusión celular con la células endógenas del la médula.
Advisors/Committee Members: [email protected] (authoremail), true (authoremailshow), Cosma, Maria Pia, 1970- (director), true (authorsendemail).
Subjects/Keywords: Bone-marrow cells; Stem cells; Retina; Regeneration; Müller glia cells; Movilización endógena; Fusión celular; Reprogramación celular; Plasticidad celular; SDF-1/CXCR4; 576
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Simonte, Giacoma, 1. (2016). Endogenous mobilization of bone-marrow cells into murine retina induces fusion-mediated reprogramming of Müller glia cells. (Thesis). Universitat Pompeu Fabra. Retrieved from http://hdl.handle.net/10803/543845
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Simonte, Giacoma, 1984-. “Endogenous mobilization of bone-marrow cells into murine retina induces fusion-mediated reprogramming of Müller glia cells.” 2016. Thesis, Universitat Pompeu Fabra. Accessed March 07, 2021.
http://hdl.handle.net/10803/543845.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Simonte, Giacoma, 1984-. “Endogenous mobilization of bone-marrow cells into murine retina induces fusion-mediated reprogramming of Müller glia cells.” 2016. Web. 07 Mar 2021.
Vancouver:
Simonte, Giacoma 1. Endogenous mobilization of bone-marrow cells into murine retina induces fusion-mediated reprogramming of Müller glia cells. [Internet] [Thesis]. Universitat Pompeu Fabra; 2016. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10803/543845.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Simonte, Giacoma 1. Endogenous mobilization of bone-marrow cells into murine retina induces fusion-mediated reprogramming of Müller glia cells. [Thesis]. Universitat Pompeu Fabra; 2016. Available from: http://hdl.handle.net/10803/543845
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Southern California
26.
Pham, Linda Kim.
Bimodal effects of bone morphogenetic proteins in prostate
cancer.
Degree: PhD, Molecular Microbiology & Immunology, 2011, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/441828/rec/1102
► This dissertation describes observations made on the effect of bone morphogenetic protein (BMP) signaling in an aggressive human prostate cancer cell line, C4-2B, two murine…
(more)
▼ This dissertation describes observations made on the
effect of bone morphogenetic protein (BMP) signaling in an
aggressive human prostate cancer cell line, C4-2B, two murine
prostate cancer cell lines, E8 and cE1, derived from the primary
site of androgen dependent and recurrent tumors of prostate cancer,
respectively, and primary cultures of murine cancer associated
fibroblasts (CAFs). We previously described that BMP7 could protect
C4-2B cells from serum starvation induced apoptosis by sustaining
Survivin expression. We further examine the mechanisms behind BMP7
mediated protection from stress induced apoptosis. When C4-2B cells
are treated with BMP7, we find that Survivin promoter activity
correlates with Smad activation and is ameliorated by dominant
negative Smad5. Furthermore JNK activity is also observed to be
sustained by BMP7 treatment in the face of serum starvation and
co-treatment with a JNK inhibitor abolished the anti-apoptotic
effect of BMP7 in a survivin independent manner. Thus we found that
anti-apoptotic activity of BMP7 is mediated by both Smad and JNK,
albeit with autonomous mechanisms. Using primary cultures of CAFs,
isolated from our conditional Pten deletion model of prostate
cancer, we tested the effect of BMP2 and 7, both of which are
upregulated during tumor growth. Interestingly, each BMP is able to
induce secretion of the cytokine,
SDF-
1/CXCL12.
SDF-
1 secretion is
correlated with Smad phosphorylation and can be blocked by Noggin
treatment. BMP treatment increases pre-spliced
SDF-
1 mRNA and
actinomycin D can block the induced secretion of
SDF-
1 by BMPs,
indicating a transcriptional modulation of
SDF-
1 expression by BMP.
Using human microvascular endothelial cells, we demonstrate that
increased
SDF-
1 levels can stimulate tube formation in vitro,
implicating a role in tumor angiogenesis. We also find that BMP can
protect CAFs from stress induced apoptosis independent of
SDF-
1.;
Thus, the study identifies a novel BMP-
SDF-
1 signaling axis as well
as a protective effect of BMP in CAFs. Finally, we examined the
effect of BMP inhibitor, Noggin, on the biology of murine prostate
cancer cell lines. In vitro data show that Noggin overexpression in
cE1 cells decreases cell proliferation while enhancing cell
migration. In contrast the in vivo data show that Noggin
overexpression increases the mass of the grafts and Ki67 staining
shows increased proliferation. We also transduced CAF cells with
Noggin and formed subcutaneous grafts in combination with cE1 or E8
cells. When E8 cells were co-injected with CAF/Noggin, larger
tumors lacking glandular structures were produced. In the case of
cE1 cells mixed with CAF/Noggin however, tumors grew mostly
resembling those with CAF/Control with evidence of decreased CD31
staining. Disparate results seen with cE1/Noggin grafts and cE1
grafts mixed with CAF/Noggin implicate a modulation of Noggin
activity by the tumor microenvironment. Similarly, the effect of
Noggin released from the CAFs appears to influence the cancer cells
differentially based on their…
Advisors/Committee Members: Roy-Burman, PradipTahara, Stanley M. (Committee Chair), Ou, Jing-Hsiung James (Committee Member), Chuong, Cheng-Ming (Committee Member).
Subjects/Keywords: Prostate Cancer; Bone Morphogenetic Proteins; BMPs; BMP2; BMP7; apoptosis; Smad; JNK; Survivin; SDF-1; angiogenesis; Noggin; C4-2B; Cancer associated fibroblasts; tumor microenvironment; E8; cE1; Pten prostate cancer mouse model
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Pham, L. K. (2011). Bimodal effects of bone morphogenetic proteins in prostate
cancer. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/441828/rec/1102
Chicago Manual of Style (16th Edition):
Pham, Linda Kim. “Bimodal effects of bone morphogenetic proteins in prostate
cancer.” 2011. Doctoral Dissertation, University of Southern California. Accessed March 07, 2021.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/441828/rec/1102.
MLA Handbook (7th Edition):
Pham, Linda Kim. “Bimodal effects of bone morphogenetic proteins in prostate
cancer.” 2011. Web. 07 Mar 2021.
Vancouver:
Pham LK. Bimodal effects of bone morphogenetic proteins in prostate
cancer. [Internet] [Doctoral dissertation]. University of Southern California; 2011. [cited 2021 Mar 07].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/441828/rec/1102.
Council of Science Editors:
Pham LK. Bimodal effects of bone morphogenetic proteins in prostate
cancer. [Doctoral Dissertation]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/441828/rec/1102

University of Alberta
27.
Landry, Breanne K.
Lipopolymer Mediated siRNA Therapy for Cancer: Focus on
Acute Myeloid Leukemia.
Degree: PhD, Department of Chemical and Materials
Engineering, 2015, University of Alberta
URL: https://era.library.ualberta.ca/files/np193d00c
► Protein silencing by small interfering RNA (siRNA) is a promising treatment strategy for cancer as over-expression of proteins is largely responsible for cancer cells’ infinite…
(more)
▼ Protein silencing by small interfering RNA (siRNA) is
a promising treatment strategy for cancer as over-expression of
proteins is largely responsible for cancer cells’ infinite
proliferation, evasion of cell death and multi-drug resistance.
However, siRNAs require a carrier as their biological instability,
negative charge and large molecular weight prevent cellular
delivery. In this thesis, I first provide a review of current
non-viral siRNA carrier strategies designed to protect and deliver
the siRNA to the cell cytoplasm for RNAi activity and then follow
with an over-view of the current state of siRNA development with
non-viral carriers specifically in leukemia. One promising cationic
polymer for siRNA delivery is high molecular weight
polyethylenimine (PEI); however, its toxicity is an obstacle for
clinical use. This thesis investigates a library of low-molecular
weight (2 kDa) PEI with hydrophobic (lipid) modifications as siRNA
carriers. The lipid modification renders this otherwise ineffective
low-toxic polymer a safe and effective delivery system for
intracellular siRNA delivery and protein silencing. We first
explore a lipid modified polymer library in adherent cells lines
targeting a model protein target, the house-keeping gene,
glyceraldehyde 3-phosphate dehydrogenase (GAPDH), and several
relevant cancer targets; P-glycoprotein (P-gp), breast cancer
resistance protein (BCRP) and survivin. These initial studies in
adherent cells demonstrated that although the exact formulations
for efficient silencing depended on the cell line and protein
target, silencing with two of the lipid-modified polymers (caprylic
and linoleic acid substitutions) were consistently effective,
suggesting that these carriers can be applied clinically.
Fine-tuning of the siRNA/polymer composition was however critical
for silencing particular targets. We then focus our efforts
specifically on Acute Myeloid Leukemia (AML), where siRNA therapy
development has lagged behind the cancers that are derived from
attachment dependent cells, as evident in the included review of
current efforts in AML siRNA therapy. We explored the feasibility
of the lipid-modified carriers in AML cell lines. Efficient siRNA
delivery and silencing of the model protein target, green
fluorescent protein (GFP), was achieved with higher functionality
than that of 25 kDa PEI, where again caprylic acid and linoleic
acid substitutions stood out as the most desirable polymer
substitutions. Further work demonstrated effective silencing of an
AML therapeutic target CXCR4, a surface expressed adhesion protein
that contributes to leukemic cell survival. The suppression of
CXCR4 as well as its ligand, SDF-1 (CXCL12), resulted in a decrease
in overall cell survival, which was largely attributed to a
decrease in cell proliferation without enhanced effects when
silencing the two targets simultaneously. The decrease in cell
numbers due to CXCR4/SDF-1 silencing occurred both in the absence
and presence of human bone marrow stromal cells (hBMSC), suggesting
that the proposed approach…
Subjects/Keywords: RNAi; Acute myeloid leukemia; SDF-1; Suspension cells; AML patient cells; THP-1; HL60; Breast cancer cells; siRNA; Adherent cells; Bone marrow stromal cells; Polyethylenimine; Non-viral carrier; KG-1; PEI; CXCR4; Cancer; Lipid; CXCL12; Proliferation; Lipopolymer
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Landry, B. K. (2015). Lipopolymer Mediated siRNA Therapy for Cancer: Focus on
Acute Myeloid Leukemia. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/np193d00c
Chicago Manual of Style (16th Edition):
Landry, Breanne K. “Lipopolymer Mediated siRNA Therapy for Cancer: Focus on
Acute Myeloid Leukemia.” 2015. Doctoral Dissertation, University of Alberta. Accessed March 07, 2021.
https://era.library.ualberta.ca/files/np193d00c.
MLA Handbook (7th Edition):
Landry, Breanne K. “Lipopolymer Mediated siRNA Therapy for Cancer: Focus on
Acute Myeloid Leukemia.” 2015. Web. 07 Mar 2021.
Vancouver:
Landry BK. Lipopolymer Mediated siRNA Therapy for Cancer: Focus on
Acute Myeloid Leukemia. [Internet] [Doctoral dissertation]. University of Alberta; 2015. [cited 2021 Mar 07].
Available from: https://era.library.ualberta.ca/files/np193d00c.
Council of Science Editors:
Landry BK. Lipopolymer Mediated siRNA Therapy for Cancer: Focus on
Acute Myeloid Leukemia. [Doctoral Dissertation]. University of Alberta; 2015. Available from: https://era.library.ualberta.ca/files/np193d00c
28.
Pham, Chantal Bich Phuong.
SDF-1/IGF-1 conjugated to a PEGylated fibrin matrix as a treatment for an ischemia reperfusion injury in skeletal muscle repair.
Degree: MSin Kinesiology, Kinesiology, 2012, University of Texas – Austin
URL: http://hdl.handle.net/2152/20054
► Ischemia/reperfusion (I/R) injury causes extensive damage to skeletal muscle, often resulting in prolonged functional deficits. This current study determines the efficacy of controlled release of…
(more)
▼ Ischemia/reperfusion (I/R) injury causes extensive damage to skeletal muscle, often resulting in prolonged functional deficits. This current study determines the efficacy of controlled release of
SDF-1α and IGF-
1 by conjugation to biodegradable, polyethylene glycol, (PEG)ylated fibrin gel matrix in skeletal muscle repair of an I/R injury. Male Sprague-Dawley rats underwent a 2-hour tourniquet induced I/R injury on their hind limbs. Twenty-four hours post injury the following treatments were administered: PEGylated fibrin gel (PEG-Fib),
SDF-
1 conjugated PEGylated fibrin gel (PEG-Fib/
SDF-
1), or dual protein IGF-
1 and
SDF-
1 conjugated PEGylated fibrin gel (PEG-Fibrin/
SDF-
1/IGF-
1. Following 14 days after injury, functional and histological evaluations were performed. There was no significant difference in maximum tetanic force production recovery between PEG-Fib and PEG-Fib/
SDF-
1 groups. However, PEG-Fib/
SDF-
1/IGF-
1 group resulted in significant improvement of force production relative to the other treatment groups. The same results were found for specific tension. Histological analysis revealed a greater distribution of small myofibers in the PEG-Fib/
SDF-
1 group than the PEG-Fib group, while the PEG-Fib/
SDF-
1/IGF-
1 group had the smallest distribution of small fibers and similar to controls (uninjured). There were also a greater number of centrally located nuclei in the PEG-Fib/
SDF-
1 group than the PEG-Fib group, while the PEG-Fib/
SDF-
1/IGF-
1 group had similar values to controls. Although these results confirm the protective role of exogenous IGF-
1,
SDF-
1 did not have an effect on skeletal muscle repair.
Advisors/Committee Members: Farrar, Roger P. (advisor), Suggs, Laura J (committee member).
Subjects/Keywords: Regenerative medicine; Muscle regeneration; Tourniquet; PEGylated fibrin; PEG; IGF-1; SDF-1
…31
Figure 2:
SDF-1 Western Blot Analysis… …x28;SDF-1) was pursued as an alternative to alleviate
the problems associated with stem… …cell therapy. Following injury, injured tissue
releases a gradient of SDF-1 and in turn SDF-1… …muscle, and liver (Kucia et al. 2004). Several pathways are activated upon
SDF-1 and… …x29; are required for effective repair (Seale et al. 2000). SDF-1 is
thought to…
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Pham, C. B. P. (2012). SDF-1/IGF-1 conjugated to a PEGylated fibrin matrix as a treatment for an ischemia reperfusion injury in skeletal muscle repair. (Masters Thesis). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/20054
Chicago Manual of Style (16th Edition):
Pham, Chantal Bich Phuong. “SDF-1/IGF-1 conjugated to a PEGylated fibrin matrix as a treatment for an ischemia reperfusion injury in skeletal muscle repair.” 2012. Masters Thesis, University of Texas – Austin. Accessed March 07, 2021.
http://hdl.handle.net/2152/20054.
MLA Handbook (7th Edition):
Pham, Chantal Bich Phuong. “SDF-1/IGF-1 conjugated to a PEGylated fibrin matrix as a treatment for an ischemia reperfusion injury in skeletal muscle repair.” 2012. Web. 07 Mar 2021.
Vancouver:
Pham CBP. SDF-1/IGF-1 conjugated to a PEGylated fibrin matrix as a treatment for an ischemia reperfusion injury in skeletal muscle repair. [Internet] [Masters thesis]. University of Texas – Austin; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/2152/20054.
Council of Science Editors:
Pham CBP. SDF-1/IGF-1 conjugated to a PEGylated fibrin matrix as a treatment for an ischemia reperfusion injury in skeletal muscle repair. [Masters Thesis]. University of Texas – Austin; 2012. Available from: http://hdl.handle.net/2152/20054

Leiden University
29.
Solingen, C. van.
The role of microRNA-126 in vascular homeostasis.
Degree: 2012, Leiden University
URL: http://hdl.handle.net/1887/19855
► This thesis details our studies assessing the role of the endothelial-enriched miRNA-126 in the regulation of vascular homeostasis. In Chapter 2 the current insight in…
(more)
▼ This thesis details our studies assessing the role of the endothelial-enriched miRNA-126 in the regulation of vascular homeostasis. In Chapter 2 the current insight in the role of miRNA-126 in vascular homeostasis is reviewed. Chapter 3 focuses on the role of miRNA-126 in ischemia induced angiogenesis, followed by Chapter 4 which describes the potential role of miRNA-126 the mobilization of vasculogenic progenitor cells upon ischemia. Both chapters utilize antagomir-technology to specifically silence miRNA-126 in vivo. This approach to silence miRNA-126 was also used in Chapter 5 to elucidate the regulatory role of miRNA-126 in vascular cell adhesion molecule-
1 expression in the kidney vasculature. Chapter 6 details our findings that circulating miRNA-126 in the periphery is not exclusively derived from endothelial cells but can also originate from platelets. Consequently, the use of aspirin has to be taken into account when relating circulating miRNA-126 levels to the progression of cardiovascular disease. Chapter 7 demonstrates that the angiogenic potential of miRNA-126 as described in Chapter 3 might reach beyond the presence of this pro-angiogenic miRNA in endothelium, but that neovascularization can also be supported by miRNA-126 expressed in circulating cells. Finally, Chapter 8 provides a summary of research presented in this thesis, presents the major conclusions that could be drawn and further discusses the role of miRNA-126 in vascular homeostasis.
Advisors/Committee Members: Zonneveld, A.J. van, Rabelink, A.J., Boer, H.C. de, Leiden University.
Subjects/Keywords: VCAM-1; Vasculogenesis; Vascular homeostasis; Vascular biology; SDF-1; Platelets; MicroRNA-126; MicroRNA; Endothelial cells; Angiogenesis
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Solingen, C. v. (2012). The role of microRNA-126 in vascular homeostasis. (Doctoral Dissertation). Leiden University. Retrieved from http://hdl.handle.net/1887/19855
Chicago Manual of Style (16th Edition):
Solingen, C van. “The role of microRNA-126 in vascular homeostasis.” 2012. Doctoral Dissertation, Leiden University. Accessed March 07, 2021.
http://hdl.handle.net/1887/19855.
MLA Handbook (7th Edition):
Solingen, C van. “The role of microRNA-126 in vascular homeostasis.” 2012. Web. 07 Mar 2021.
Vancouver:
Solingen Cv. The role of microRNA-126 in vascular homeostasis. [Internet] [Doctoral dissertation]. Leiden University; 2012. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/1887/19855.
Council of Science Editors:
Solingen Cv. The role of microRNA-126 in vascular homeostasis. [Doctoral Dissertation]. Leiden University; 2012. Available from: http://hdl.handle.net/1887/19855
30.
Panousopoulos, S-G.
Προγνωστική και διαγνωστική αξία παραγόντων στρώματος του όγκου και αποπτωτικών μορίων στον καρκίνο του παγκρέατος.
Degree: 2010, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)
URL: http://hdl.handle.net/10442/hedi/25399
► In this study, the genotype and allelic frequencies of stromal and apoptotic tumoral factors of pancreatic adenocarcinoma were explored, identified, investigated and studied, as to…
(more)
▼ In this study, the genotype and allelic frequencies of stromal and apoptotic tumoral factors of pancreatic adenocarcinoma were explored, identified, investigated and studied, as to search on the effect of their polymorphisms in pancreatic cancer patients. Therefore 80 pancreatic cancer patients as well as 160 healthy individuals as controls, were included in this search. The molecular factors and their polymorphisms, included the SDF-1, chemokine and genotype and allelic frequencies of caspase-9 1263A/G as well as survivin-31G/C polymorphisms. The PCR-RFLPs was the method applied-employed to search for these stromal factors, and evaluate their effect. Advanced T stage and lymph node metastases were statistically correlated with the “GA+AA”: genotype group of patients, while a clear trend for significance was observed when distant metastatic disease was present. Also, allelic frequencies of allele “A”, of SDF-1, confers an increased susceptibility to pancreatic cancer as well as the possibility of aggressive features of this malignancy. This study, comes as the first one to certify this. Further to the above, the caspase-9/“G” allele analysis, as well, confers, the increased susceptibility to pancreatic cancer development and the survivin ”C” carriage status could be possibly related to aggressive features of the pancreatic cancer.
H παρούσα μελέτη, αφορά στην έρευνα, αναγνώριση και σπουδή των συχνοτήτων/ακολουθιών των γονοτύπων και αλληλίων των παραγόντων του στρώματος και των αποπτωτικών μορίων του όγκου, για τον καρκίνο του παγκρέατος. Περαιτέρω, διερευνήθηκαν τα αποτελέσματα των πολυμορφισμών αυτών των παραγόντων, σε ογδόντα (80) ασθενείς (Ομάδα A) με καρκίνο του παγκρέατος, διαφόρου σταδιοποίησης, εκ της Α! Προπαιδευτικής Χειρουργικής Κλινικής του Παν/μίου Αθηνών. Επιπλέον, ως μάρτυρες, χρησιμοποιήθηκαν εκατόν εξήντα (160) υγιή άτομα (Ομάδα Β) (από δεξαμενή DNA ). Kαι οι δύο ομάδες ερευνήθηκαν με PCR-RFLPs, για το γονότυπο και τις αλληλιακές συχνότητες του γονιδίου SDF-1,της κασπάσης-9 1263A/G και πολυμορφισμών της σουρβιβίνης-31G/C. Προχωρημένο στάδιο (Τ) της νόσου και λεμφαδενικές μεταστάσεις (Ν),παρουσίασαν στατιστικά σημαντική σχέση με τους ασθενείς γονότυπου “GA+AA” ενώ ταυτόχρονα καθαρή τάση σημαντικότητας, παρατηρήθηκε σε ασθενείς με απομεμακρυσμένες μεταστάσεις. Επίσης, αλληλιακές ακολουθίες/συχνότητες του αλληλίου “A” του παράγοντος SDF-1, συμβαδίζουν με την ηυξημένη επιδεκτικότητα στον παγκρεατικό καρκίνο αλλά και την έκφαση των επιθετικών ιδιοτήτων του αδενοκαρκινώματος του παγκρέατος. Ως φαίνεται, η μελέτη αυτή ενδεχομένως είναι η πρώτη πού πιστοποιεί αυτούς τους συσχετισμούς. Η ανάλυση του αλληλίου “G” της κασπάσης-9, επίσης φαίνεται ότι συσχετίζεται με την ηυξημένη επιδεκτικότητα στην ανάπτυξη παγκρεατικού καρκίνου, αλλά και η σουρβιβίνη “C”-φορέας-πιθανότατα σχετίζεται με τις επιθετικές ιδιότητες του παγκρεατικού καρκίνου.
Subjects/Keywords: Καρκίνος παγκρέατος; Κασπάση-9; Πολυμορφισμοί; Σουρβιβίνη; Pancreatic cancer; Caspase-9; Polymorphisms; Survivin; SDF-1; CXCL12
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Panousopoulos, S. (2010). Προγνωστική και διαγνωστική αξία παραγόντων στρώματος του όγκου και αποπτωτικών μορίων στον καρκίνο του παγκρέατος. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/25399
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Panousopoulos, S-G. “Προγνωστική και διαγνωστική αξία παραγόντων στρώματος του όγκου και αποπτωτικών μορίων στον καρκίνο του παγκρέατος.” 2010. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed March 07, 2021.
http://hdl.handle.net/10442/hedi/25399.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Panousopoulos, S-G. “Προγνωστική και διαγνωστική αξία παραγόντων στρώματος του όγκου και αποπτωτικών μορίων στον καρκίνο του παγκρέατος.” 2010. Web. 07 Mar 2021.
Vancouver:
Panousopoulos S. Προγνωστική και διαγνωστική αξία παραγόντων στρώματος του όγκου και αποπτωτικών μορίων στον καρκίνο του παγκρέατος. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2010. [cited 2021 Mar 07].
Available from: http://hdl.handle.net/10442/hedi/25399.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Panousopoulos S. Προγνωστική και διαγνωστική αξία παραγόντων στρώματος του όγκου και αποπτωτικών μορίων στον καρκίνο του παγκρέατος. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2010. Available from: http://hdl.handle.net/10442/hedi/25399
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
◁ [1] [2] ▶
.