You searched for subject:(Transforming Growth Factor beta1 pharmacology 60).
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1.
Moore, Lakisha Dionne.
Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.
Degree: PhD, 2008, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,233 
► Overexpresssion of transforming growth factor (TGF)-[beta] has been implicated in promoting immune suppression, tumor angiogenesis, tumor cell migration, and invasion in many cancers including carcinoma…
(more)
▼ Overexpresssion of transforming growth factor (TGF)-[beta] has been implicated in
promoting immune suppression, tumor angiogenesis, tumor cell migration, and invasion
in many cancers including carcinoma of the breast. Thus, targeted downregulation of
TGF-[beta]1 expression in breast cancer in situ and determination of its implications
potentially could provide new treatment approaches for disease management. siRNA
constructs targeting TGF-[beta]1 were validated and used to develop clonal derivatives of the
MDA-MB-435 metastatic breast cancer cell line. Inhibition of TGF-[beta]1 expression in
MDA-MB-435 cells showed decrease in migration and invasion in vitro with an increase
in proliferation. In vivo analysis indicated a 90% decrease in the number of mice
bearing macroscopic lung metastases. Analysis of TGF-[beta] signaling pathways in the clonal
derivatives showed a decrease in Smad2 activation and an increase in AKT and ERK
activation.
Analysis of TGF-[beta] signaling in the tumor microenvironment was performed using
co-culture assays consisting of both MDA-MB 435 tumor cells and fibroblasts. Early
experiments involving analysis of gene expression in a breast cancer xenograft model
showed an increase in TGF-[beta]1 and MMP expression in the tumor stroma over tumor
progression. Co-culture experiments using Boyden chambers indicated increased
expression of TGF-[beta]1, MMP-9, MMP-2, T[beta]R1 and T[beta]R2 in the tumor cells.
Interestingly, there was a significant decrease in TGF-[beta]1, MMP-2, T[beta]R1 and T[beta]R2
expression in fibroblasts that were co-cultured with tumor cells. Experiments using
conditioned media also showed a decrease in fibroblasts and tumor cell differentiation
through decreases in alpha-smooth muscle actin and cytokeratin 18, respectively.
Therapeutic efficacy was determined using rAAV to administer TGF-[beta]1 siRNA
intra-tumorally. Results confirmed that the AAV6 serotype was effectively able to
transduce the tumor cells both in vitro and in vivo. RT-PCR data confirmed that TGF-[beta]1,
MMP-9 and MMP-2 were effectively decreased in the tumor injected with rAAV-TGF[beta]si
when compared to the rAAV-GFP injected tumors. Macroscopic lung metastases were
decreased in the treated group; however microscopic metastases were still present. Lung
weights also show a decrease, however, the differences were not statistically significant.
Better understanding of the molecular pathways involved in TGF-[beta] signaling will
help to advance the development of targeted therapeutics along with improvements in
delivery mechanics. Through our studies we have shown that inhibition of TGF-[beta] can
effectively reduce cancer metastasis; we have identified secondary pathways active in
mammary cancer neoplastic progression which may be targeted in combination to give a
synergistic effect and tested alternative methods of delivery.
xi, 109 p. : ill., digital, PDF file
Joint Health Sciences
Transforming Growth Factor-beta Breast Cancer Metastasis Gene Therapy Adeno-Associated Virus …
Advisors/Committee Members: Ponnazhagan, Selvarangan, Chang, Chenbei <br>, Feng, Xu <br>, Serra, Rosa <br>, Siegal, Gene P. <br>, Thottassery, Jaideep.
Subjects/Keywords: Breast Neoplasms – genetics <; br>; Neoplasm Metastasis <; br>; RNA Interference <; br>; Transforming Growth Factor beta1 – genetics <; br>; Transforming Growth Factor beta1 – metabolism
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APA (6th Edition):
Moore, L. D. (2008). Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,233
Chicago Manual of Style (16th Edition):
Moore, Lakisha Dionne. “Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,233.
MLA Handbook (7th Edition):
Moore, Lakisha Dionne. “Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.” 2008. Web. 12 Dec 2019.
Vancouver:
Moore LD. Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,233.
Council of Science Editors:
Moore LD. Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,233
2.
Roarty, Kevin Patrick.
The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis.
Degree: PhD, 2008, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,337
► Breast cancer is the second most common cancer worldwide behind lung cancer, affecting women of all ages, races, ethnicities, and socioeconomic strata. Concerted efforts have…
(more)
▼ Breast cancer is the second most common cancer worldwide behind lung cancer,
affecting women of all ages, races, ethnicities, and socioeconomic strata. Concerted
efforts have been made to understand this heterogeneous disease from the clinical stage
down to the molecular level. Importantly, it has become clear that an understanding of
the normal biology of the breast at all stages of development is needed to gain insight into
how alterations in normal regulatory networks contribute to the initiation and
development of breast cancer.
TGF-[beta] plays a role in growth and patterning of the mammary gland and
alterations in its signaling exhibit biphasic effects during tumorigenesis. Here, we
identified Wnt5a as a downstream effector of TGF-[beta] within the mammary gland.
Furthermore, we established a requirement of Wnt5a for 1) orchestrating proper
mammary gland development at multiple stages and 2) TGF-[beta]-mediated inhibition of
ductal growth. We went on to establish that TGF-[beta] and Wnt5a act to inhibit the
canonical Wnt/[beta]-catenin pathway in the mammary gland, having implications on
development, stem cell dynamics, and tumorigenesis. Together, this dissertation provides a novel link between TGF-[beta] and Wnt pathways that might extend beyond the mammary
gland.
viii, 114 p. : ill., digital, PDF file
Cell Biology
Joint Health Sciences
mammary gland wnt5a tgf-beta
UNRESTRICTED
Advisors/Committee Members: Serra, Rosa A., Chang, Chenbei <br>, Frost, Andra R. <br>, Miller, Michael A. <br>, Welch, Danny R..
Subjects/Keywords: Gene Expression Regulation, Developmental <; br>; Mammary Glands, Animal – growth & development <; br>; Mammary Glands, Animal – metabolism <; br>; Transforming Growth Factor beta1 – pharmacology <; br>; Wnt Proteins – metabolism
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APA ·
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APA (6th Edition):
Roarty, K. P. (2008). The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,337
Chicago Manual of Style (16th Edition):
Roarty, Kevin Patrick. “The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,337.
MLA Handbook (7th Edition):
Roarty, Kevin Patrick. “The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis.” 2008. Web. 12 Dec 2019.
Vancouver:
Roarty KP. The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,337.
Council of Science Editors:
Roarty KP. The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,337
3.
Seo, Hwa-Seon.
The role of TGF[beta] signaling in skeletal development.
Degree: PhD, 2008, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,338
► Each skeletal element is essential for body movement along with the joints, muscles, tendons and ligaments. They also protect internal organs and serve as a…
(more)
▼ Each skeletal element is essential for body movement along with the joints,
muscles, tendons and ligaments. They also protect internal organs and serve as a
reservoir for hematopoietic stem cells and minerals. To accomplish these multiple tasks,
the size and shape of the skeletal elements need to be carefully designed during
development of the embryo. Skeletal formation in vertebrae is a complex developmental
processes controlled by dynamic and well-balanced interactions between a number of
molecular signals. Intensive efforts in the past several decades have made substantial
progress in understanding molecular and cellular mechanisms of skeletal development.
Despite the fact that TGF[beta] signaling has been considered as a potential trigger for
the onset of skeletal development, it has not been studied well. Here, we show important
roles for TGF[beta] signaling in skeletal development using a transgenic mouse model in
which Tgfbr2 is specifically deleted in cells that will be programmed to become various
components of the skeleton. Primarily, discoveries in this study show the precise role of
TGF[beta] signaling in specific stages of skeletal development. Defining the role of TGF[beta]
signaling in specific stages, cells or tissues has been difficult because of the complexity
of skeletal development. Secondly, results presented here provide a novel function of
TGF[beta] signaling in skeletal development, which has not been previously suggested.
Finally, evidence provided in this study shows multiple roles of TGF[beta] in
intramembranous and endochondral bone formation.
viii, 120 p. : ill., digital, PDF file
Cell Biology
Joint Health Sciences
TGFbeta signaling chondrogenesis endochondral bone formation intramembranous bone formation osteoblast differentiation skeletal development
UNRESTRICTED
Advisors/Committee Members: Serra, Rosa A., Yoder, Bradly K. <br>, Chang, Chenbei <br>, Marques, Guillermo <br>, Murphy-Ullrich, Joanne.
Subjects/Keywords: Bone and Bones – abnormalities <; br>; Homeodomain Proteins – genetics <; br>; Joints – abnormalities <; br>; Mesoderm – embryology <; br>; Protein-Serine-Threonine Kinases – Metabolism <; br>; Receptors, Transforming Growth Factor beta – metabolism <; br>; Transforming Growth Factor beta1 – physiology
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Seo, H. (2008). The role of TGF[beta] signaling in skeletal development. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,338
Chicago Manual of Style (16th Edition):
Seo, Hwa-Seon. “The role of TGF[beta] signaling in skeletal development.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,338.
MLA Handbook (7th Edition):
Seo, Hwa-Seon. “The role of TGF[beta] signaling in skeletal development.” 2008. Web. 12 Dec 2019.
Vancouver:
Seo H. The role of TGF[beta] signaling in skeletal development. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,338.
Council of Science Editors:
Seo H. The role of TGF[beta] signaling in skeletal development. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,338
University of Illinois – Urbana-Champaign
4.
Xu, Jing.
Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system.
Degree: MS, 0408, 2010, University of Illinois – Urbana-Champaign
URL: http://hdl.handle.net/2142/16963
► In this work, we explored a thick in vitro 3-D cell culture model with layered structure and applied transforming growth factor-beta1 (TGF-??1) on the top…
(more)
▼ In this work, we explored a thick in vitro 3-D cell culture model with layered structure and applied
transforming growth factor-
beta1 (TGF-??1) on the top of the 3-D culture to induce the conversion from normal fibroblasts to myofibroblasts and expression of a marker protein, alpha-smooth muscle actin (??-SMA). The cell response with TGF-??1 stimulation was captured with immunofluorescence staining (IF) and confocal microscopy imaging of ??-SMA in each cell embedded layer. Our results revealed the spatial-temporal profiles of the conversion from normal fibroblasts to myofibroblasts in 3-D culture upon TGF-??1stimulation. The conversion starting time, speed and saturation plateau are closely related to TGF-??1 concentration. Based on these experimental results, we successfully developed a mathematical model, which incorporates diffusion of
growth factors and cell activation responses to describe the dynamic cell response to
growth factors across the 3-D culture depth and predict the spatial-temporal profile of the fibroblast conversion within the culture. In summary, we present here a handy experimental and computational tool for researches on tumor signaling pathways, and provide some guidance for studies on diffusion of protein factors or drugs in 3-D tissue environment.
Advisors/Committee Members: Insana, Michael F. (advisor).
Subjects/Keywords: myofibroblasts; transforming growth factor-beta1; alpha-smooth muscle actin; diffusion; confocal microscopy imaging; immunofluorescence staining
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❌
APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Xu, J. (2010). Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/16963
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):
Xu, Jing. “Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system.” 2010. Thesis, University of Illinois – Urbana-Champaign. Accessed December 12, 2019.
http://hdl.handle.net/2142/16963.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Xu, Jing. “Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system.” 2010. Web. 12 Dec 2019.
Vancouver:
Xu J. Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2010. [cited 2019 Dec 12].
Available from: http://hdl.handle.net/2142/16963.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Xu J. Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system. [Thesis]. University of Illinois – Urbana-Champaign; 2010. Available from: http://hdl.handle.net/2142/16963
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
North-West University
5.
Campbell, Berenice.
Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell
.
Degree: 2010, North-West University
URL: http://hdl.handle.net/10394/4739
► Pigmentation disorders occur in multiple conditions (Hakozaki et al., 2006:105). Although many modalities of treatments are available, none are completely satisfactory (Briganti et al., 2003:101).…
(more)
▼ Pigmentation disorders occur in multiple conditions (Hakozaki et al., 2006:105). Although many
modalities of treatments are available, none are completely satisfactory (Briganti et al.,
2003:101). Two cytokines normally present in the skin, transforming growth factor–beta1
(TGF–81) and tumour necrosis factor–alpha (TNF–9), have been shown to inhibit melanin
synthesis (Martinez–Esparza, 2001:972).
The stratum corneum has been commonly accepted as the main barrier to percutaneous
absorption. Many techniques have been applied to overcome this barrier properties and to
enhance penetration with varying success (Pellet et al., 1997:92).
The objective of this study was to investigate the topical delivery of the above mentioned
peptide drugs with aid of the Pheroid drug delivery system. Pheroid technology is a
delivery system that promotes the absorption and increases the efficacy of dermatological,
biological and oral medicines in various pharmacological groups (Grobler et al., 2008:4).
Pheroid entraps drugs with high efficiency and delivers them with remarkable speed to target
sites (Grobler, 2004:4). In order to avoid degradation of these peptides, bestatin hydrochloride
(an aminopeptidase inhibitor), was used (Lkhagvaa et al., 2008:386).
Topical drug delivery was achieved by means of vertical Franz cell diffusion studies performed
over a 6 and 12 h period. ELISA (enzyme linked immunosorbent assay) detection was used to
detect cytokine concentrations. Entrapped cytokine solutions were monitored by confocal laser
scanning microscopy (CLSM). Upon removal of donor and receptor compartments, skin discs
were subjected to tape stripping in order to establish the amount of active present within the
stratum corneum and epidermis as well as the remaining dermis (Pellet et al., 1997:92).
When comparing the two studies with each other, it is evident that the diffused concentration
values obtained with PBS (phosphate buffer solution, pH 7.4) was lower than that obtained with
the Pheroid drug delivery system. Both cytokine concentrations were successfully delivered
topically as a minimum of concentrations for both actives were detected. This positive result
was confirmed as well by the amount of active detected in stratum corneum–epidermis and
epidermis–dermis solutions.
Subjects/Keywords: Pigmentation;
Topical delivery;
Pheroid;
Transforming growth factor-beta1;
Tumour necrosis factor-alpha;
Bestatin;
Tape stripping;
Pigmentasie;
Topikale aflewering;
Transformerende groei faktor-beta1;
Tumor nekrosis faktor-alpha;
Bestatien;
Bandstroping
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❌
APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Campbell, B. (2010). Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell
. (Thesis). North-West University. Retrieved from http://hdl.handle.net/10394/4739
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):
Campbell, Berenice. “Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell
.” 2010. Thesis, North-West University. Accessed December 12, 2019.
http://hdl.handle.net/10394/4739.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Campbell, Berenice. “Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell
.” 2010. Web. 12 Dec 2019.
Vancouver:
Campbell B. Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell
. [Internet] [Thesis]. North-West University; 2010. [cited 2019 Dec 12].
Available from: http://hdl.handle.net/10394/4739.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Campbell B. Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell
. [Thesis]. North-West University; 2010. Available from: http://hdl.handle.net/10394/4739
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
McGill University
6.
Rafiei, Shahrzad.
Talin : a novel inducible antagonist of transforming growth factor-beta 1 (TGF-[beta]1) signal transduction.
Degree: MS, Division of Experimental Medicine., 2007, McGill University
URL: http://digitool.library.mcgill.ca/thesisfile100203.pdf
► The survival of breast cancer patients declines when tumors are invasive and have an increased possibility of metastasizing to distal sites. Transforming Growth Factor-beta (TGF-beta)…
(more)
▼ The survival of breast cancer patients declines when tumors are invasive and have an increased possibility of metastasizing to distal sites. Transforming Growth Factor-beta (TGF-beta) suppresses breast cancer formation by preventing cell cycle progression in mammary epithelial cells. However, at late stage of mammary carcinogenesis, due to genetic and epigenetic alterations, TGF-beta loses its cytostatic actions, and contributes to tumor invasion by promoting cell proliferation, Actin cytoskeletal reorganization, as well as Epithelial to Mesenchymal Transition (EMT). Despite the key role of TGF-beta1 in tumor suppression as well as tumor progression, the molecular mechanisms underlying the conversion of TGF-beta form an inhibitor of proliferation in mammary breast cancer cells to an inducer of their cell growth and EMT have not been fully elucidated. Thus, acquiring a basic knowledge on the mechanism of TGF-beta regulating its target genes and its contribution to cancer progression may highlight new avenues for cancer therapy development. This prompted us to further investigate and identify TGF-beta-inducible genes that may be involved in TGF-beta biological responses during tumorigenesis.
In this thesis, we identified Talin as a novel TGF-beta1 target gene that acts as an antagonist to inhibit TGF-beta-mediated cell growth arrest and transcriptional activity in mammary cancer cell line, MCF-7. Searching for new partners of activated Smads, we found that TGF-beta1 induces Talin translocation from cytosol to the plasma membrane where Talin physically interacts with the TGF-beta1 signaling components, the Smads and the receptors. Furthermore, we observed that TGF-beta1 stimulation leads to the formation of Actin stress fibers where Talin was detected at the end of these stress fibers. Taken all together, the obtained data show that TGF-beta1 positively induced expression of Talin and suggests a role for Talin, which acts as a negative feedback loop to control TGF-beta biological responses.
Subjects/Keywords: Talin.; Transforming Growth Factor beta1 – antagonists & inhibitors.
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7.
Rafael Braga Petito.
Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural.
Degree: 2008, Fundação Oswaldo Cruz
URL: http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224
► Neural fibrosis is one of the causes of deformities during leprosy, which remains a major global health problem. Neural degeneration progresses after the patient healing…
(more)
▼ Neural fibrosis is one of the causes of deformities during leprosy, which remains a major global health problem. Neural degeneration progresses after the patient healing and, as suggested by others, the Schwann cells (SC) are involved in the degeneration and regeneration of the nerve. Our group showed, in a human Schwannoma lineage (ST88-14), increased mRNA levels of the cytokine TGF-b1 and its receptors after Mycobacterium leprae (ML) stimulus. Since TGF-b1 neutralization reduces fibrosis, and this cytokine promotes transdifferentiation of the SC into myofibroblast, which in turn, overproduce extracellular matrix (ECM) components, resulting in neural degeneration, the aim of this study was to investigate the possible role of ML, PGL-I (lipidic component of ML cell wall) and TGF-b1 on the neural ECM expression. ST88-14 cells were stimulated with ML or PGL-I to evaluate TGF-b1, its mRNA and its receptor (TGFRII) expression. This cytokine levels were measured in these supernatants cultures. In order to evaluate myofibroblast transdifferentiation (a-actin smooth muscle; aSMA) and ECM secretion/deposition and proteins structural form, ST88-14 were stimulated with recombinant human TGF-b1, ML or PGL-I. TGF-b1 and SMA expression were analyzed in patients nerve biopsies without pathological changes or with varying degrees of fibrosis and inflammation. Our results showed that ML or PGL-I stimulation induced a rapid increase in TGF-b1 mRNA expression, followed by a decline that maintained until 6 hours. This cytokine secretion seems to accompany mRNA expression. However, after 6 hours of stimulation, TGF-b1 secretion seems gradually to return to baseline levels and to rise again after 7 days of stimulation. The intracellular cytokine expression increased in cells stimulated with ML, but the opposite took place when PGL-I was the stimulus. ML or PGL-I also up regulated the TGFRII expression. After 7 days of TGF-b1 stimulation, we noticed the increased expression of collagen IV, laminin, fibronectin and tenascin, and, in some cases, the modulation of their structural forms of some of these proteins. Moreover, TGF-b1 also induced transdifferentiation of SC into myofibroblasts. In leprosy biopsies patients, the TGF-b1 expression seems to pass from the axon to SC. For the first time, we showed the SMA expression in blood vessels, perineurium and some endoneurial cells in nerve biopsies with fibrosis presence. These results suggest a TGF-b1 involvement in cellular modulation response to ML and PGL-I, and SC-myofibroblastic transdifferentiation, which could contribute to fibrosis and, consequently, to neural degeneration.
A fibrose neural é uma das causas de deformidades durante o curso crônico da hanseníase, a qual ainda é um grande problema de saúde pública mundial. A degeneração neural progride mesmo depois da cura do paciente e as células de Schwann (CS) estão envolvidas na degeneração e regeneração neural. A produção de citocinas pela CS parece estar relacionada ao processo de degeneração e regeneração do nervo. Em trabalho…
Advisors/Committee Members: Euzenir Nunes Sarno.
Subjects/Keywords: BIOLOGIA MOLECULAR; Mycobacterium leprae; Fibrose/complicações; Hanseníase; Saúde Pública; Fator Transformador de Crescimento beta1/análise; Mycobacterium leprae; Fibrosis/Complications; Leprosy; Public Health; Transforming Growth Factor beta1/analysis
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APA ·
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MLA ·
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CSE |
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to Zotero / EndNote / Reference
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APA (6th Edition):
Petito, R. B. (2008). Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural. (Thesis). Fundação Oswaldo Cruz. Retrieved from http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224
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):
Petito, Rafael Braga. “Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural.” 2008. Thesis, Fundação Oswaldo Cruz. Accessed December 12, 2019.
http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Petito, Rafael Braga. “Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural.” 2008. Web. 12 Dec 2019.
Vancouver:
Petito RB. Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural. [Internet] [Thesis]. Fundação Oswaldo Cruz; 2008. [cited 2019 Dec 12].
Available from: http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Petito RB. Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural. [Thesis]. Fundação Oswaldo Cruz; 2008. Available from: http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toledo Health Science Campus
8.
Elkareh, Jihad Victor.
Molecular Mechanism of Fibrosis and Central Role of
Cardiotonic Steroids in Uremic Cardiomyopathy.
Degree: PhD, College of Graduate Studies, 2008, University of Toledo Health Science Campus
URL: http://rave.ohiolink.edu/etdc/view?acc_num=mco1213115467
► It has been recognized that patients with chronic renal failure eventually develop diastolic dysfunction, cardiac hypertrophy and systemic oxidant stress along with increases in…
(more)
▼ It has been recognized that patients with
chronic renal failure eventually develop diastolic dysfunction,
cardiac hypertrophy and systemic oxidant stress along with
increases in circulating concentrations of the cardiotonic steroid,
marinobufagenin (MBG) in uremic cardiomyopathy. Because of this, we
performed 5/6th partial nephrectomy in rats to study experimental
renal failure (PNx), MBG infusion, PNx after immunization against
MBG, and concomitant PNx and adrenalectomy. We also studied 5/6th
partial nephrectomy as a potential experimental renal failure model
in mice. Next, we speculated a relationship between decreases Fli-1
expression and increases in collagen production following exposure
to MBG. Therefore, we examined Fli-1 knockdown mice and compared it
to wild type mice. Physiological measurements with a Millar
catheter and immunohistochemistry were performed. In vitro studies
were then pursued with cultured isolated cardiac fibroblasts, human
dermal fibroblasts, as well as a cell line derived from renal
fibroblasts. First, in rats, we observed that
PNx after immunization against MBG as well as concomitant PNx and
adrenalectomy had similar blood pressure as PNx but less cardiac
hypertrophy, diastolic dysfunction, and cardiac fibrosis. Second,
in mice, the 5/6 nephrectomy resulted in impairment of both active
and passive left ventricular relaxation at four weeks as well as
progressive fibrosis in the heart. Third, the Fli-1 knockdown mice
showed greater amounts of cardiac collagen expression and fibrosis
compared to wild type before and after 4 weeks of experimental
renal failure induced by 5/6th nephrectomy.We realized that
stimulation of cultured cardiac fibroblasts with MBG could be
prevented by administration of inhibitors of tyrosine
phosphorylation, Src activation, EGFR transactivation, and N-acetyl
cysteine. Furthermore, in response to MBG, decreases in nuclear
Fli-1 accompanied increases in procollagen expression. Finally, we
observed that exposure of cardiac fibroblasts to MBG was associated
with a rapid translocation of PKCd to the nucleus that appeared to
peak at about 15 minutes as determined with confocal
immunofluorescence and Western blot. Taken
together, these data suggest that MBG directly induces increases in
collagen expression by fibroblasts in a process involving Fli-1 and
PKCd, and is in part responsible for the cardiac fibrosis seen with
experimental renal failure.
Advisors/Committee Members: Shapiro, Joseph (Committee Chair).
Subjects/Keywords: Pharmacology; Surgery; cardiomyopathy; cardiotonic steroids; renal failure; marinobufagenin; fibrosis; transforming growth factor TGF-&946
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APA (6th Edition):
Elkareh, J. V. (2008). Molecular Mechanism of Fibrosis and Central Role of
Cardiotonic Steroids in Uremic Cardiomyopathy. (Doctoral Dissertation). University of Toledo Health Science Campus. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=mco1213115467
Chicago Manual of Style (16th Edition):
Elkareh, Jihad Victor. “Molecular Mechanism of Fibrosis and Central Role of
Cardiotonic Steroids in Uremic Cardiomyopathy.” 2008. Doctoral Dissertation, University of Toledo Health Science Campus. Accessed December 12, 2019.
http://rave.ohiolink.edu/etdc/view?acc_num=mco1213115467.
MLA Handbook (7th Edition):
Elkareh, Jihad Victor. “Molecular Mechanism of Fibrosis and Central Role of
Cardiotonic Steroids in Uremic Cardiomyopathy.” 2008. Web. 12 Dec 2019.
Vancouver:
Elkareh JV. Molecular Mechanism of Fibrosis and Central Role of
Cardiotonic Steroids in Uremic Cardiomyopathy. [Internet] [Doctoral dissertation]. University of Toledo Health Science Campus; 2008. [cited 2019 Dec 12].
Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1213115467.
Council of Science Editors:
Elkareh JV. Molecular Mechanism of Fibrosis and Central Role of
Cardiotonic Steroids in Uremic Cardiomyopathy. [Doctoral Dissertation]. University of Toledo Health Science Campus; 2008. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1213115467
9.
Lopes, Roberto Iglesias.
Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos.
Degree: PhD, Urologia, 2014, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/
;
► Introdução: A alteração dos níveis normais de marcadores séricos e urinários ocorre na presença de dano renal associado à uropatia obstrutiva. Valores séricos e e…
(more)
▼ Introdução: A alteração dos níveis normais de marcadores séricos e urinários ocorre na presença de dano renal associado à uropatia obstrutiva. Valores séricos e e urinários de TGF beta1 e CA 19-9 ainda não foram avaliados em modelo experimental de uropatia obstrutiva. Material e Métodos: Ratos foram divididos em sete grupos: referência, sham operation, nefrectomia unilateral, ligadura completa de ureter unilateral, obstrução parcial de ureter unilateral, obstrução parcial de ambos ureteres, nefrectomia unilateral associada à obstrução parcial do ureter contralateral. Morfometria renal e ureteral, concentrações séricas e urinárias de TGF beta1 e CA 19-9 e expressão tecidual renal de CA 19-9 foram analisadas. A correlação destes marcadores com os grupos submetidos a obstrução completa, obstrução parcial ou sem obstrução foi realizada. Resultados: Achados anatomopatológicos correlacionaram-se positivamente à intensidade da obstrução ureteral e negativamente aos níveis urinários de CA 19-9. Subexpressão acentuada do CA 19-9 foi observada em unidades renais com obstrução completa. Não foram encontradas diferenças estatisticamente significativas para os marcadores TGF beta1 urinário, TGF beta1 sérico e para o CA 19-9 sérico Conclusões: O CA 19-9 urinário correlacionou-se negativamente com o grau de obstrução ureteral. A análise imuno-histoquímica demonstrou a expressão do CA 19-9 no citoplasma das células epiteliais tubulares, sugerindo produção renal do marcador. O TGF beta1 sérico e urinário não apresentaram modificações de acordo com o grau de severidade e tempo de obstrução, o que pode estar relacionado a remodelamento renal menos intenso em resposta à uropatia obstrutiva nestes ratos
Introduction: Abnormal levels of serum and urinary markers occur in the presence of renal damage associated to obstructive uropathy. Urinary and serum TGFbeta1 and CA 19- 9 have not yet been evaluated in an experimental model of obstructive uropathy. Material and Methods: Rats were divided into seven groups: reference, sham operation, unilateral nephrectomy, complete unilateral ureteral obstruction, partial unilateral ureteral obstruction, partial bilateral ureteral obstruction, and unilateral nephrectomy with contralateral partial ureteral obstruction. Kidney and ureter morphometry, TGFbeta1 and CA 19-9 serum and urinary concentrations and CA 19-9 renal tissue expression were analysed. Correlation of these markers to complete, partial obstruction or unobstructed groups was performed. Results: Pathological findings correlated positively with the degree of ureteral obstruction, but negatively with urinary CA 19-9 levels. Marked underexpression of CA 19-9 was observed in kidneys with complete ureteral obstruction. No statistically significant differences were found for urinary and serum TGFbeta1 and also for serum CA 19-9. Conclusions: Urinary CA 19-9 correlated negatively with ureteral obstruction grade. Immunohistochemistry depicted CA 19-9 expression on epithelial tubular cells cytoplasm, suggesting renal origin. Serum and urinary…
Advisors/Committee Members: Denes, Francisco Tibor.
Subjects/Keywords: Antígeno CA 19-9; CA 19-9 antigen; Fator de crescimento transformador beta 1; Obstrução ureteral; Ratos Wistar; Transforming growth
factor beta1; Ureter; Ureter; Ureteral obstruction; Wistar rats
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MLA ·
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to Zotero / EndNote / Reference
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APA (6th Edition):
Lopes, R. I. (2014). Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;
Chicago Manual of Style (16th Edition):
Lopes, Roberto Iglesias. “Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos.” 2014. Doctoral Dissertation, University of São Paulo. Accessed December 12, 2019.
http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;.
MLA Handbook (7th Edition):
Lopes, Roberto Iglesias. “Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos.” 2014. Web. 12 Dec 2019.
Vancouver:
Lopes RI. Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos. [Internet] [Doctoral dissertation]. University of São Paulo; 2014. [cited 2019 Dec 12].
Available from: http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;.
Council of Science Editors:
Lopes RI. Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos. [Doctoral Dissertation]. University of São Paulo; 2014. Available from: http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;
10.
Gilbert, Rebekah (Rebekah Sims).
The role of TGF-β receptors in the induction of mucosal tolerance
.
Degree: PhD, 2011, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,945
► Oral tolerance, defined as the immunologic state of systemic and mucosal unresponsiveness to an antigen, is an essential function of the mucosal immune system. Although…
(more)
▼ Oral tolerance, defined as the immunologic state of systemic and mucosal unresponsiveness
to an antigen, is an essential function of the mucosal immune system. Although
antigen presentation has been found to play an important role in oral tolerance, T
cells are known to be the effector immune cells that perpetrate this state. Recent studies
found that antigen-specific T regulatory (Treg) cells are important in the induction and
maintenance of oral tolerance. The extrathymic development of these Tregs depends on
the presence of TGF-β1 during the differentiation process. However, it has also been
shown that oral tolerance could be induced in TGF-β1 knockout mice. Given this contradicting
information, we sought to further the understanding of the role of TGF-β1 in
high- and low-dose oral tolerance induction by focusing on the expression and function
of TGFβRII, the signaling component of the oligomeric TGF-β receptor complex, on
CD4+ T cells of the systemic (spleen) and relevant mucosal [Peyer’s patches (PPs), mesenteric
lymph nodes (MLNs), and small intestinal lamina propria (iLP)] immune tissues.
We hypothesized that TGFβRII on CD4+ T cells is required for both low- and high-dose
oral tolerance induction and therefore focused on the role the expression of this receptor
by CD4+ T cells plays at early time points after exposure to the tolerogenic dose(s) of antigen.
We found that the expression of TGFβRII by CD4+ T cells is upregulated at the
site of antigen uptake -the PPs- soon after exposure to the tolerizing dose of antigen. Further,
we showed that these cells diminish in the PPs and increase in the MLNs and iLP
soon after re-exposure to the antigen in the presence of mucosal adjuvant. Also, by employing
the CD4 dominant negative TGFβRII transgenic mouse model in which
TGFβRII signaling in CD4+ T cells has been abrogated, we found that the proper function
of TGFβRII is required for the induction of oral tolerance. Further analysis is necessary
to tease out the exact function of these PP TGFβRII+ CD4+ T cells in the induction
of oral tolerance.
1 online resource (xii, 69 p. : ill., digital, PDF file)
Microbiology;
Joint Health Sciences;
Mucosal immune system
oral tolerance
T cell
TGF-β
TGF-β receptor
T regulatory cell
UNRESTRICTED
Advisors/Committee Members: Fujihashi, Kohtaro, Burrows, Peter D.<br>, Lorenz, Robinna G.<br>, Michalek, Suzanne M.<br>, Weaver, Casey T..
Subjects/Keywords: Antigens – immunology<; br>;
Immune Tolerance<; br>;
Immunity, Mucosal – immunology<; br>;
Receptors, Transforming Growth Factor beta<; br>;
T-Lymphocytes, Regulatory<; br>;
Transforming Growth Factor beta
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Gilbert, R. (. S. (2011). The role of TGF-β receptors in the induction of mucosal tolerance
. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,945
Chicago Manual of Style (16th Edition):
Gilbert, Rebekah (Rebekah Sims). “The role of TGF-β receptors in the induction of mucosal tolerance
.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,945.
MLA Handbook (7th Edition):
Gilbert, Rebekah (Rebekah Sims). “The role of TGF-β receptors in the induction of mucosal tolerance
.” 2011. Web. 12 Dec 2019.
Vancouver:
Gilbert R(S. The role of TGF-β receptors in the induction of mucosal tolerance
. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,945.
Council of Science Editors:
Gilbert R(S. The role of TGF-β receptors in the induction of mucosal tolerance
. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,945
11.
Lucas, Jason Anthony.
Counterregulatory roles of transforming growth factor (TGF)-[beta] and a trial natruiretic peptide (ANP) in pressure overload-induced cardiac remodeling and fibrosis.
Degree: PhD, 2009, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,570
► Pressure overload stress (eg. hypertension or aortic stenosis) results in excessive cardiac fibrosis, changes in left ventricular (LV) geometry, and disruption of LV contractility, ultimately…
(more)
▼ Pressure overload stress (eg. hypertension or aortic stenosis) results in
excessive cardiac fibrosis, changes in left ventricular (LV) geometry, and
disruption of LV contractility, ultimately leading to heart failure. We hypothesize
that transforming growth factor-beta (TGF-[Beta]), a pro fibrogenic factor, and atrial
natriuretic peptide (ANP), an anti fibrogenic factor, interact directly in a
counterregulatory manner to balance the production of extracellular matrix (ECM)
under pressure overload induced cardiac stress or hypoxia-induced pulmonary
vascular adaptation. In this report, we examine structural and functional
responses of the intact heart to pressure overload stress in vivo. We then utilize
isolated rat pulmonary artery smooth muscle cells (PASMC) and mouse cardiac
fibroblasts (CF) to delineate on the cellular level the counterregulatory roles of
TGF[Beta] and ANP/cGMP/protein kinase G (PKG) in determining stress responses in
vitro.
First, we utilized a DnTGF[Beta]RII mouse model to define the contribution of
TGF[Beta] signaling to the phenotype of cardiac remodeling and fibrosis in response
to pressure overload. We demonstrated that inhibition of TGF-[Beta] signaling
attenuates pressure overload-induced interstitial non-myocyte proliferation and
collagen deposition with subsequent development of LV dilation and systolic
dysfunction.
Second, we demonstrated that ANP has an anti-fibrogenic effect on
PASMC treated with TGF-[Beta]. ANP and cGMP suppressed the TGF-[Beta] stimulated
ECM gene expression by interfering with Smad signaling through a protein
kinase G (PKG)–dependent mechanism. The most striking finding of this study is
that ANP and cGMP inhibit TGF-[Beta]1-induced nuclear translocation of pSmad2
and pSmad3, but not the phosphorylation of Smad2 and Smad3 in PASMCs,
thus defining a novel molecular mechanism by which ANP signaling intercepts
the TGF-[Beta] signaling pathway and blocks TGF-[Beta]-induced ECM expression.
Finally, we demonstrated a precise site of “molecular merging” of profibrogenic
(TGF[Beta]/Smad) and anti-fibrogenic (ANP/cGMP/PKG) pathways in CFs:
PKG induced hyper-phosphorylation of Smad3 protein, with resultant failure of
nuclear translocation of pSmad3 and consequent inhibition of TGF[Beta]/Smad
induced ECM gene expression. Thus, we have demonstrated cross talk between
ANP and TGF-[Beta] signaling pathways in CFs in vitro such that ANP/cGMP, through
a PKG dependent mechanism, block induction of ECM expression by TGF-[Beta]1.
1 online resource (xvi, 137 p. : ill., digital, PDF file)
Physiology and Biophysics
Joint Health Sciences;
Transforming growth factor-beta
atrial natruretic factor
cardiac fibroblast
cardiac fibrosis and remodeling
signal transduction
UNRESTRICTED
Advisors/Committee Members: Oparil, Suzanne, Bellis, Susan<br>, Blalock, J. Edwin<br>, Chen, Yiu-Fai<br>, Perry, Gilbert<br>, Murphy-Ullrich, Joanne.
Subjects/Keywords: Atrial Natriuretic Factor – metabolism<; br>;
Cardiomyopathy, Dilated – physiopathology<; br>;
Heart – physiopathology<; br>;
Signal Transduction – physiology<; br>;
Transforming Growth Factor beta – antagonists & inhibitors
Vasodilation – physiology<; br>;
Ventricular Dysfunction, Left – physiopathology
Record Details
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Lucas, J. A. (2009). Counterregulatory roles of transforming growth factor (TGF)-[beta] and a trial natruiretic peptide (ANP) in pressure overload-induced cardiac remodeling and fibrosis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,570
Chicago Manual of Style (16th Edition):
Lucas, Jason Anthony. “Counterregulatory roles of transforming growth factor (TGF)-[beta] and a trial natruiretic peptide (ANP) in pressure overload-induced cardiac remodeling and fibrosis.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,570.
MLA Handbook (7th Edition):
Lucas, Jason Anthony. “Counterregulatory roles of transforming growth factor (TGF)-[beta] and a trial natruiretic peptide (ANP) in pressure overload-induced cardiac remodeling and fibrosis.” 2009. Web. 12 Dec 2019.
Vancouver:
Lucas JA. Counterregulatory roles of transforming growth factor (TGF)-[beta] and a trial natruiretic peptide (ANP) in pressure overload-induced cardiac remodeling and fibrosis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,570.
Council of Science Editors:
Lucas JA. Counterregulatory roles of transforming growth factor (TGF)-[beta] and a trial natruiretic peptide (ANP) in pressure overload-induced cardiac remodeling and fibrosis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,570
Texas A&M University
12.
McMillin, Matthew Alexander.
The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis.
Degree: 2013, Texas A&M University
URL: http://hdl.handle.net/1969.1/151843
► Hepatic encephalopathy (HE) is a neurological complication that arises due to liver dysfunction and is associated with increased circulating ammonia and a systemic immune response.…
(more)
▼ Hepatic encephalopathy (HE) is a neurological complication that arises due to liver dysfunction and is associated with increased circulating ammonia and a systemic immune response. Treatment paradigms have attempted to minimize the metabolic and inflammatory consequences of liver failure. However, investigations into the specific cell signaling mechanisms between the liver and brain that induce these pathological processes are currently lacking. Both TGF?1 and Shh are known to be upregulated in the liver and present in the circulation following liver damage. These studies employed the azoxymethane (AOM) model of acute liver failure in mice, the bile duct ligation (BDL) model of minimal HE in rats, and patients with liver cirrhosis who had HE to study cell signaling and pathological processes present during HE. Studies of specific cellular signaling mechanisms were performed in isolated primary neurons and immortalized brain endothelial cells. All pharmacological manipulations of hedgehog signaling, TGF? signaling, and clodronate-liposome depletion of microglia were performed in AOM mice. Gli1 was upregulated in AOM, BDL, and HE patient cortices. Shh was upregulated in the liver and serum during HE, but had no effect on neurological decline. Liver TGF?1 signaling was upregulated and had increased expression in cortical neurons. TGF?1 suppressed neuronal Gli1 via SMAD3. The use of neutralizing antibodies against TGF? generated neuroprotection during HE. The BBB was disrupted during AOM-induced HE and neutralizing antibodies against TGF? significantly reduced permeability. Studies using bEnd.3 cells found that TGF?1 suppressed Claudin-5 and increased MMP9 through a SMAD3-dependent mechanism. Depletion of microglia with clodronate liposomes in AOM mice was protective. Cortical CCL3/CCR1 axis signaling was elevated during HE and was reduced with neutralizing antibodies against TGF?. Also, treatment with neutralizing antibodies against TGF? reduced microgliosis and microglia activation. CCL3 KO mice had no changes in neurological decline compared to wild-type mice. Elevation of Gli1 or suppression of TGF?1 was neuroprotective during HE. TGF?1 increased BBB permeability and generated microglia activation and microgliosis during HE though this effect was not through the CCL3/CCR1 signaling axis. Gli1 or TGF?1 may be therapeutic targets for the treatment and management of HE.
Advisors/Committee Members: DeMorrow, Sharon (advisor), Di Patre, Pier L (committee member), Meininger, Cynthia (committee member), Sanchez, Russell (committee member).
Subjects/Keywords: Hepatic Encephalopathy; Transforming Growth Factor Beta
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APA ·
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APA (6th Edition):
McMillin, M. A. (2013). The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151843
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):
McMillin, Matthew Alexander. “The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis.” 2013. Thesis, Texas A&M University. Accessed December 12, 2019.
http://hdl.handle.net/1969.1/151843.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
McMillin, Matthew Alexander. “The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis.” 2013. Web. 12 Dec 2019.
Vancouver:
McMillin MA. The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis. [Internet] [Thesis]. Texas A&M University; 2013. [cited 2019 Dec 12].
Available from: http://hdl.handle.net/1969.1/151843.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
McMillin MA. The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis. [Thesis]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151843
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
IUPUI
13.
Rhodes, Steven David.
Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects.
Degree: 2014, IUPUI
URL: http://hdl.handle.net/1805/3793
► Indiana University-Purdue University Indianapolis (IUPUI)
Skeletal manifestations including short stature, osteoporosis, kyphoscoliosis, and tibial dysplasia cumulatively affect approximately 70% of patients with neurofibromatosis type 1…
(more)
▼ Indiana University-Purdue University Indianapolis (IUPUI)
Skeletal manifestations including short stature, osteoporosis, kyphoscoliosis, and tibial dysplasia cumulatively affect approximately 70% of patients with neurofibromatosis type 1 (NF1). Tibial pseudarthrosis, the chronic non-union of a spontaneous fracture, is a debilitating skeletal malady affecting young children with NF1. These non-healing fractures respond poorly to treatment and often require amputation of the affected limb due to limited understanding of the causative mechanisms.
To better understand the cellular and molecular pathogenesis of these osseous defects, we have established a new mouse model which recapitulates a spectrum of skeletal pathologies frequently observed in patients with NF1. Nf1flox/-;Col2.3Cre mice, harboring Nf1 nullizygous osteoblasts on a Nf1+/- background, exhibit multiple osseous defects which are closely reminiscent of those found in NF1 patients, including runting (short stature), bone mass deficits, spinal deformities, and tibial fracture non-union.
Through adoptive bone marrow transfer studies, we have demonstrated that the Nf1 haploinsufficient hematopoietic system pivotally mediates the pathogenesis of bone loss and fracture non-union in Nf1flox/-;Col2.3Cre mice. By genetic ablation of a single Nf1 allele in early myeloid development, under the control of LysMCre, we have further delineated that Nf1 haploinsufficient myeloid progenitors and osteoclasts are the culprit lineages mediating accelerated bone loss. Interestingly, conditional Nf1 haploinsufficiency in mature osteoclasts, induced by CtskCre, was insufficient to trigger enhanced lytic activity. These data provide direct genetic evidence for Nf1’s temporal significance as a gatekeeper of the osteoclast progenitor pool in primitive myelopoiesis.
On the molecular level, we found that transforming growth factor-beta1 (TGF-β1), a primary mediator in the spatiotemporal coupling of bone remodeling, is pathologically overexpressed by five- to six- fold in both NF1 patients and in mice. Nf1 deficient osteoblasts, the principal source of TGF-β1 in the bone matrix, overexpress TGF-β1 in a gene dosage dependent fashion. Moreover, p21Ras dependent hyperactivation of the Smad pathway accentuates responses to pathological TGF-β1 signals in Nf1 deficient bone cells. As a proof of concept, we demonstrate that pharmacologic TβRI kinase inhibition can rescue bone mass defects and prevent tibial fracture non-union in Nf1flox/-;Col2.3Cre mice, suggesting that targeting TGF-β1 signaling in myeloid lineages may provide therapeutic benefit for treating NF1 skeletal defects.
Advisors/Committee Members: Yang, Feng-Chun, Clapp, D. Wade, Robling, Alexander G., Bidwell, Joseph P..
Subjects/Keywords: Neurofibromatosis type 1; Bone; Osteoporosis; Pseudarthrosis; Mouse model; Osteoclasts; Transforming growth factor-beta1; Neurofibromatosis – Research; Neurofibromatosis – Genetic aspects; Osteoporosis – Alternative treatment – Research – Methodology; Osteoporosis – Prevention; Pseudarthrosis – Research – Analysis; Mice – Diseases – Pathophysiology – Research; Osteoclasts – Research; Hematopoiesis – Research; Bone cells – Research; Bones – Growth; Spine – Abnormalities; Nervous system – Diseases; Bone marrow – Transplantation – Research; Transforming growth factors-beta – Research
Record Details
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Rhodes, S. D. (2014). Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/3793
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):
Rhodes, Steven David. “Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects.” 2014. Thesis, IUPUI. Accessed December 12, 2019.
http://hdl.handle.net/1805/3793.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Rhodes, Steven David. “Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects.” 2014. Web. 12 Dec 2019.
Vancouver:
Rhodes SD. Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects. [Internet] [Thesis]. IUPUI; 2014. [cited 2019 Dec 12].
Available from: http://hdl.handle.net/1805/3793.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Rhodes SD. Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects. [Thesis]. IUPUI; 2014. Available from: http://hdl.handle.net/1805/3793
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Western Ontario
14.
Siraj, Sadia.
A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity.
Degree: 2017, University of Western Ontario
URL: https://ir.lib.uwo.ca/etd/4856
► Chronic musculoskeletal pain results in significant personal, economic, and social burden. Early identification and intervention in those people with acute pain that are likely to…
(more)
▼ Chronic musculoskeletal pain results in significant personal, economic, and social burden. Early identification and intervention in those people with acute pain that are likely to transition into a state of chronicity can prevent the onset of chronic pain before it emerges and becomes resistant to treatment. This study investigated the potential stress biomarkers associated with acute pain and disability and how those associations are influenced by early life adversities.
Stress level was determined according to the plasma level of stress biomarkers (cortisol, BDNF, TGFB1) and self-report measures of stress following musculoskeletal traumatic events. The magnitude and direction of associations of cortisol and BDNF with self-reported stress markers provided supportive evidence for further exploration of cortisol and BDNF as acute stress biomarkers. The results of the study also supported the moderating role of adverse childhood experiences on the associations between self-reported distress and stress biomarkers.
Subjects/Keywords: Chronic pain; acute musculoskeletal trauma; Hypothalamic-Pituitary-Adrenal axis (HPA axis); stress biomarkers; Cortisol; Brain-derived neurotrophic factor (BDNF); Transforming growth factor beta1 (TGFB1); early life adversity.; Physical Therapy; Preventive Medicine; Rehabilitation and Therapy; Trauma
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APA (6th Edition):
Siraj, S. (2017). A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/4856
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):
Siraj, Sadia. “A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity.” 2017. Thesis, University of Western Ontario. Accessed December 12, 2019.
https://ir.lib.uwo.ca/etd/4856.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Siraj, Sadia. “A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity.” 2017. Web. 12 Dec 2019.
Vancouver:
Siraj S. A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity. [Internet] [Thesis]. University of Western Ontario; 2017. [cited 2019 Dec 12].
Available from: https://ir.lib.uwo.ca/etd/4856.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Siraj S. A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity. [Thesis]. University of Western Ontario; 2017. Available from: https://ir.lib.uwo.ca/etd/4856
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
15.
Tang, Yi, Ph.D.
The role of transforming growth factor beta-1 in bone remodeling.
Degree: PhD, 2009, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,405
► Bone remodeling depends on the precise coordination of bone resorption by the osteoclasts and bone formation by the osteoblasts. It is proposed that osteoclastic bone…
(more)
▼ Bone remodeling depends on the precise coordination of bone resorption by the osteoclasts and bone formation by the osteoblasts. It is proposed that osteoclastic bone resorption releases factors to initiate bone formation, thereby, coupling the bone resorption and formation.
Mesenchymal stem cells (MSCs) are progenitors of osteoblasts. Recruitment of MSCs in response to osteoclastic bone resorption may be an initial step for bone formation during bone remodeling process. Therefore, we have established an in vitro osteoclastic bone resorption system. Bone resorption condition medium have been tested to identify the factor inducing the migration of human bone marrow mesechymal stem cells (hBMMSCs). TGF[beta]1, in the bone resorption condition medium has been shown to be a primary factor inducing the migration of hBMMSCs. Indeed, osteoclastic bone resorption releases and activates TGF[beta]1 from the bone matrix. TGF[beta]-Smads signaling mediates, whereas, TGF[beta]-RhoA signaling confines the migration of hBMMSCs induced by the bone resorption condition medium. These data suggest that TGF[beta]1 may couple the bone resorption and the migration of MSCs during bone remodeling.
To determine the role of TGF[beta]1 in recruiting MSCs in vivo, we have detected the MSCs on bone remodeling sites in TGF[beta]1 null mice. Depletion of TGF[beta]1 reduces MSCs counts on bone remodeling sites. Alternatively, data from tracing the BrdU-labeled hBMMSCs, which have been transplanted into mouse bone marrow cavity, indicate that
deletion of TGF[beta]1 inhibits the recruitment of these labeled MSCs to the bone remodeling sites. Similarly, block of TGF[beta] signaling with a TGF[beta]1 receptor type I kinase inhibitor also reduces the recruitment of MSCs. Correlated with these observations, knockout of TGF[beta]1 causes a significant bone loss. These data suggest that TGF[beta]1 may couple bone resorption and formation through recruiting MSCs to the bone remodeling sites.
Bone metastasis is a bone remodeling related disease. TGF[beta]1 released by bone resorption increases the formation of bone lesions in breast cancer patients. Since TGF[beta]1 is also a critic regulatory factor in bone remodeling, general inhibition of TGF[beta] signaling may lead to bone defect. Therefore, specific block of TGF[beta] signaling in breast cancer cells should be a better therapeutic choice. We found that expression of Smad7 in breast cancer cells significantly increases cell-cell adhesion and inhibits the invasiveness of cancer cells. Therefore, these findings may also provide a potential therapy for inhibiting bone metastasis.
xi, 156 p. : ill., digital, PDF file
Pathology
Joint Health Sciences
Bone Remodeling Osteoblast Osteoclast Breast Cancer Smads
UNRESTRICTED
Advisors/Committee Members: Cao, Xu, Feng, Xu<br>Frand, Stuart J.<br>Klug, Christopher A.<br>Murphy-Ullrich, Joanne.
Subjects/Keywords: beta Catenin – metabolism<; br>; Bone Regeneration – drug effects<; br>; Cadherins – metabolism<; br>; Cell Membrane – metabolism<; br>; Multiprotein Complexes – metabolism<; br>; Smad7 Protein – metabolism<; br>; Transforming Growth Factor beta – metabolism
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Manager
APA (6th Edition):
Tang, Yi, P. D. (2009). The role of transforming growth factor beta-1 in bone remodeling. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,405
Chicago Manual of Style (16th Edition):
Tang, Yi, Ph D. “The role of transforming growth factor beta-1 in bone remodeling.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,405.
MLA Handbook (7th Edition):
Tang, Yi, Ph D. “The role of transforming growth factor beta-1 in bone remodeling.” 2009. Web. 12 Dec 2019.
Vancouver:
Tang, Yi PD. The role of transforming growth factor beta-1 in bone remodeling. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,405.
Council of Science Editors:
Tang, Yi PD. The role of transforming growth factor beta-1 in bone remodeling. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,405
16.
Katre, Ashwini A.
Ozone and lung fibrosis.
Degree: M.S.P.H., 2009, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,485
► Ozone is an extremely reactive gas molecule composed of three oxygen atoms. The ground-level ozone is formed when nitrogen oxides and volatile organic compounds, released…
(more)
▼ Ozone is an extremely reactive gas molecule composed of three oxygen atoms. The
ground-level ozone is formed when nitrogen oxides and volatile organic compounds, released
mainly from burning of gasoline or coal, come into contact with sunlight. Ozone
is also generated and used in industrial settings such as purification of drinking water,
waste treatment, deodorization of gases, bleaching of wood pulp. Therefore, many industrial
workers are exposed to relatively high concentrations of ozone through their working
environment. Although governmental organizations have set up the exposure limit no
more than 0.1ppm for 8 hour work, the concentrations of ozone in the many work environments
can reach much higher levels than the standards.
Ozone exposure is associated with many health effects in human, involving different organ
systems; however, the major target of ozone toxicity is the respiratory system. Both
clinical studies and epidemiological studies have shown that ozone exposure induces various health problems in respiratory system. Studies show that industrial workers have
a higher risk of developing adult–onset asthma and decreased pulmonary function as
compared with general population. Although no pathological data are available regarding
whether ozone exposure induces lung fibrosis in human, decreased forced vital capacity,
is observed among ozone exposure workers, indicating that ozone exposure causes restrictive
lung diseases.
In addition to clinical and epidemiology studies, many studies have been conducted using
different animal models to address health effects of ozone exposure. Numerous studies
have shown that ozone increases collagen and [Alpha]-smooth muscle actin ([Alpha]-SMA) and plasminogen
activator inhibitor 1 (PAI-1) synthesis and deposition in the lungs indicating that
ozone induces lung fibrosis. Although it has been well documented that ozone exposure
induces lung fibrosis, the underlying mechanism remains unclear.
In this study we demonstrate that transforming growth factor-[Beta] (TGF-[Beta]) has a pivotal
role in the pathogenesis of ozone induced lung fibrosis. Inhibition of TGF-[Beta] signaling
attenuates the ozone induced lung fibrosis. These findings provide new insights into the
molecular mechanism whereby ozone induces lung fibrosis, which will enable the design
of more efficacious therapeutic agents for the treatment of ozone-related occupational
diseases.
M.S.P.H.
vii, 49 p. : ill., digital, PDF file
Public Health
Fibrosis
Transforming Growth Factor-[Beta]
Collagen
Smooth Muscle Actin
Plasminogen Activator Inhibitor 1
UNRESTRICTED
Advisors/Committee Members: Liu, Rui-Ming, Fanucchi, Michelle<br>, Lungu, Claudiu.
Subjects/Keywords: Actins<; br>;
Collagen – metabolism<; br>;
Ozone – toxicity<; br>;
Plasminogen Activator Inhibitor 1<; br>;
Pulmonary Fibrosis – chemically induced<; br>;
Pulmonary Fibrosis – pathology<; br>;
Transforming Growth Factor beta
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Manager
APA (6th Edition):
Katre, A. A. (2009). Ozone and lung fibrosis. (Masters Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,485
Chicago Manual of Style (16th Edition):
Katre, Ashwini A. “Ozone and lung fibrosis.” 2009. Masters Thesis, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,485.
MLA Handbook (7th Edition):
Katre, Ashwini A. “Ozone and lung fibrosis.” 2009. Web. 12 Dec 2019.
Vancouver:
Katre AA. Ozone and lung fibrosis. [Internet] [Masters thesis]. University of Alabama – Birmingham; 2009. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,485.
Council of Science Editors:
Katre AA. Ozone and lung fibrosis. [Masters Thesis]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,485
17.
Mukherjee, Sudipto.
Retinal pigment epithelial cells and the insulin-like growth factor system in proliferative vitreoretinopathy.
Degree: PhD, 2007, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,257
► The goal of this study was to determine the influence, if any, of the insulin-like growth factors (IGFs) on retinal pigment epithelial (RPE) cell tractional…
(more)
▼ The goal of this study was to determine the influence, if any, of the insulin-like
growth factors (IGFs) on retinal pigment epithelial (RPE) cell tractional force generation
and the contributions of vitreous insulin-like growth factor binding proteins (IGFBPs)
towards control of IGF activity. Another objective was to evaluate RPE cells as a
potential source of all six high-affinity IGFBPs and to determine if IGFBP biosynthesis is
modulated in concert with phenotype changes and growth factor stimuli known to be
present in disease.
RPE generate tractional forces in response to IGF-I and -II with IGF-I being the
more potent stimulus. Differential RPE responses to non-IGFBP binding analogue,
R3IGF-I reflected minor amounts of endogenous IGFBP production. IGFBPs -2, -3 and -5
were effective inhibitors of both ligands while IGFBP-6 reduced cell responses to IGF-II
only. IGFBP direct effects on the cells were binding protein-specific in that only IGFBP-
1 had detectable stimulatory effects and IGFBPs -3, -4, -5 and -6 inhibited RPE
responses.
Changes in RPE phenotype occur very early in culture and can be defined by
differential expression of cytoskeletal proteins. Normal RPE are immunoreactive for
cytokeratin 18 and negative for cytokeratin 19, vimentin and [alpha] smooth muscle actin
([alpha]SMA). At seven days (7d) in culture, RPE cells express cytokeratins 18, 19 and
vimentin. After 35 days (35d) in continuously proliferating cultures, RPE cells expresscytokeratin 19, vimentin and [alpha]SMA. RT-PCR studies revealed that normal RPE express
IGFBP-2 -3, -4, -5 and -6, but not IGFBP-1. Following introduction in to culture, ‘early
reactive’ (7d) and ‘myofibroblastic’ (35d) RPE possess detectable message for IGFBP-3,
-5 and -6. However, Northern, Western ligand and Western blots suggest that functional
IGFBP production by these RPE is limited to IGFBP-5 and this secretory profile is not
under the influence of IGF system ligands. These data provide compelling evidence that
RPE cells produce as well as respond to IGF system components, signals that drive the
fibrocontractive process in proliferative vitreoretinopathy.
xi, 64 p. : ill., digital, PDF file.
Vision Science
Optometry
RPE IGF IGFBP Proliferative Vitreoretinopathy
UNRESTRICTED
Advisors/Committee Members: Guidry, Clyde, Curcio, Christine A.<br>, Keyser, Kent T.<br>, Kraft, Timothy W.<br>, Wang, Shu-Zhen.
Subjects/Keywords: Insulin-Like Growth Factor Binding Proteins <; br>; Insulin-Like Growth Factor I – pharmacology <; br>; Insulin-Like Growth Factor II – pharmacology <; br>; Pigment Epithelium of Eye – drug effects
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APA ·
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Manager
APA (6th Edition):
Mukherjee, S. (2007). Retinal pigment epithelial cells and the insulin-like growth factor system in proliferative vitreoretinopathy. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,257
Chicago Manual of Style (16th Edition):
Mukherjee, Sudipto. “Retinal pigment epithelial cells and the insulin-like growth factor system in proliferative vitreoretinopathy.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,257.
MLA Handbook (7th Edition):
Mukherjee, Sudipto. “Retinal pigment epithelial cells and the insulin-like growth factor system in proliferative vitreoretinopathy.” 2007. Web. 12 Dec 2019.
Vancouver:
Mukherjee S. Retinal pigment epithelial cells and the insulin-like growth factor system in proliferative vitreoretinopathy. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,257.
Council of Science Editors:
Mukherjee S. Retinal pigment epithelial cells and the insulin-like growth factor system in proliferative vitreoretinopathy. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,257
NSYSU
18.
Kao, Ying-hsien.
Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis.
Degree: PhD, Biological Sciences, 2009, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053
► Liver fibrosis, a major medical problem with significant morbidity and mortality, is considered as a wound-healing response to a variety of chronic stimuli. It is…
(more)
▼ Liver fibrosis, a major medical problem with significant morbidity and
mortality, is considered as a wound-healing response to a variety of chronic
stimuli. It is characterized by an excessive deposition of extracellular
matrix (ECM) proteins, which disrupts the normal architecture of liver and
ultimately leads to pathophysiological damage to liver. Hepatoma-derived
growth factor (HDGF), a
growth factor originally purified from hepatoma
cells, is highly expressed in fetal hepatocytes and hepatoma. It is known to
play multifunctional roles in mitogenesis, organogenesis, embryogenesis,
and tumorigenesis. Its expression correlates with the proliferating state of
hepatocellular carcinoma (HCC) and serves as a prognostic
factor. Since
liver fibrosis frequently occurs prior to HCC development, the specific aim
of this study is to investigate the role of HDGF in the progression of liver
fibrosis by using animal models of mice receiving either bile duct ligation
surgery or carbon tetrachloride administration. Quantitative real-time PCR
and Western blotting analysis showed a significant elevation of HDGF
expression in both models. HDGF levels correlated with progression of
liver fibrosis in a time-dependent manner as well as paralleled with the
expression of other two fibrotic markers,
transforming growth factor-b1
(TGF-b1) and pro-collagen type I, in fibrotic livers. Intriguingly, the
over-expressed HDGF protein was localized mainly in perivenous
hepatocytes of fibrotic livers. Besides, adenovirus-mediated HDGF gene
delivery potentiated the production of TGF-b1 and pro-collagen type I,
thereby enhancing the intrahepatic collagen matrix deposits as evidenced
by Sirius red stain and morphometrical analysis. In cultured hepatocytes,
TGF-b1 and HDGF mutually up-regulated their de novo synthesis only
when grown on collagen-coated matrix, strongly suggesting that the
TGF-b1- and/or HDGF-driven pro-fibrogenic signaling is
collagen-dependent and a vicious circle may exist at the initial stage of
hepatic fibrogenesis. Moreover, administration with recombinant HDGF
stimulated BrdU uptake and synthesis of both a-smooth muscle actin and
pro-collagen type I in cultured hepatic stellate cells, implicating that a
mode of paracrinal action lies between these two cell types. In conclusion,
HDGF plays a pro-fibrogenic role during liver fibrosis and blockade of
HDGF pathway may potentially constitute the preventive or therapeutic
strategies for chronic liver diseases.
Advisors/Committee Members: Ming-hong Tai (committee member), Jiin-haur Chuang (chair), Tsung-hui Hu (chair), David Chao (committee member), Hung-tu Huang (chair).
Subjects/Keywords: hepatoma-derived growth factor; liver fibrosis; hepatocytes; transforming growth factor-beta
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MLA ·
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APA (6th Edition):
Kao, Y. (2009). Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053
Chicago Manual of Style (16th Edition):
Kao, Ying-hsien. “Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis.” 2009. Doctoral Dissertation, NSYSU. Accessed December 12, 2019.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053.
MLA Handbook (7th Edition):
Kao, Ying-hsien. “Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis.” 2009. Web. 12 Dec 2019.
Vancouver:
Kao Y. Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis. [Internet] [Doctoral dissertation]. NSYSU; 2009. [cited 2019 Dec 12].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053.
Council of Science Editors:
Kao Y. Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis. [Doctoral Dissertation]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053
19.
Maynard, Craig Lueland.
IL-10-competent regulatory T cells: development, phenotype and function.
Degree: PhD, 2007, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,529
► In order to avoid chronic cell activation and inflammation the immune system has developed numerous mechanisms that cooperate to induce and/or maintain what is known…
(more)
▼ In order to avoid chronic cell activation and inflammation the immune system has
developed numerous mechanisms that cooperate to induce and/or maintain what is known
as peripheral tolerance. One such mechanism involves active suppression of immune
cells by regulatory CD4 T cells (Treg). Treg can generally be categorized as either
natural Treg that develop intrathymically during positive selection and suppress the
function of autoreactive T cells, or adaptive Treg that develop in the periphery following
antigenic stimulation. One widely studied subset of adaptive Treg is the T regulatory 1
(Tr1) cell that is able to suppress immune responses in vivo and in vitro in an IL-10-
dependent manner. Although it now appears that Tr1 develop in vitro in the absence of
natural CD25+ Treg, it is still unknown whether or not there exists any in vivo lineage
relationship between the two subsets. Despite certain overlapping phenotypic and
functional features between natural Treg and Tr1, the specific role of Tr1 in
immunoregulation has not been defined.
Natural Treg were originally identified by expression of the IL-2 receptor-[Alpha] chain
(CD25), a transiently expressed marker of activation. This means that a CD4+CD25+ T
cell population is a heterogeneous mix of natural Treg and one or more effector subsets.
Consequently, it is still unclear which specific cells within this population are responsible
for the regulatory phenomena observed. The transcription factor Foxp3 has been
identified as the natural Treg lineage specification factor, and despite being a nuclear protein, is currently the most effective marker for this subset. Isolation of Tr1 has been
even more difficult primarily because no unique surface marker has been identified.
Instead, Tr1 are often studied following ex vivo isolation of CD4 T cells induced in an
antigen-specific manner to secrete large quantities of IL-10.
We have developed IL-10 and Foxp3 dual-reporter mice that allow us to
simultaneously identify cells that express these two genes. Using this model we found
that in vivo in the steady state, based solely on co-ordinate or differential expression of
these genes, there exists three bona fide subsets of regulatory T cells – Foxp3+IL-10-,
Foxp3-IL-10+, and Foxp3+IL-10+ - all of which can develop extrathymically from naïve
precursors. Despite very striking polarized distribution of the three subsets, all subsets
were found in every lymphoid and non-lymphoid compartment examined. In contrast to
what has been suggested for Tr1 cells in particular, we found no role for IL-10 or ICOS
in the development of either any of the two IL-10+ subsets. Instead, TGF-[Beta] appears to be
a critical player in the developmental cascade of all three subsets.
x, 117 p. : ill., digital, PDF file
Microbiology
Joint Health Sciences;
Interleukin-10
Regulatory T Cell
Tr1
Immune Homeostasis
UNRESTRICTED
Advisors/Committee Members: Weaver, Casey T., Chaplin, David D.<br>, Elson, Charles O. III<br>, Lorenz, Robinna G.<br>, Timares, Laura<br>, Walter, Mark R..
Subjects/Keywords: Cell Differentiation – immunology<; br>;
Forkhead Transcription Factors – immunology<; br>;
Inflammation – immunology<; br>;
Interleukin-10 – metabolism<; br>;
T-Lymphocyte Subsets – cytology<; br>;
Transforming Growth Factor beta
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Maynard, C. L. (2007). IL-10-competent regulatory T cells: development, phenotype and function. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,529
Chicago Manual of Style (16th Edition):
Maynard, Craig Lueland. “IL-10-competent regulatory T cells: development, phenotype and function.” 2007. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,529.
MLA Handbook (7th Edition):
Maynard, Craig Lueland. “IL-10-competent regulatory T cells: development, phenotype and function.” 2007. Web. 12 Dec 2019.
Vancouver:
Maynard CL. IL-10-competent regulatory T cells: development, phenotype and function. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2007. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,529.
Council of Science Editors:
Maynard CL. IL-10-competent regulatory T cells: development, phenotype and function. [Doctoral Dissertation]. University of Alabama – Birmingham; 2007. Available from: http://contentdm.mhsl.uab.edu/u?/etd,529
20.
Lee, Yun Kyung.
Late developmental plasticity in the T helper 17 lineage.
Degree: PhD, 2009, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,916
► CD4 T cells are a principal component of the adaptive immune system that is required for the efficient elimination of foreign antigens, but dysregulated CD4…
(more)
▼ CD4 T cells are a principal component of the adaptive immune system that is
required for the efficient elimination of foreign antigens, but dysregulated CD4 T cells
responses may result in autoimmune and chronic inflammatory diseases. The
differentiation of effector CD4 T cells is directed by cytokines elicited by pathogendriven
innate immune responses. Therefore the coordinated innate and adaptive immune
responses provide an efficient system for host protection. Our understanding of distinct
differentiated CD4 T cells has recently expanded with the discovery of the Th17 lineage,
a new subset of effector CD4 T cells that has been implicated in chronic immune
responses, host defense and autoimmunity. Th17 cells are characterized by expression of
the unique cytokines, IL-17A and IL-17F, and the representative transcription factors,
ROR!t and ROR", which are required for their differentiation in response to TGF-# and
IL-6. Despite distinct developmental signals, Th17 cells were originally proposed to be a
branch of Th1 lineage because there are interesting overlaps between the two lineages.
Developing Th17 cells upregulate an inducible receptor IL-23R that binds IL-23, whereas
developing Th1 cells induce IL-12R#2 expression that binds to IL-12. Both inducible
receptors pair with the constitutively expressed IL-12R#1 chain and drive late events
downstream of early Th17 or Th1 lineage commitment. Mice deficient for other Th1
lineage factor (IFN!-/-, IFN!R-/-, IL-12R#2-/-, IL-12p35-/- or STAT1-/-) are susceptible to
autoimmunity, whereas deficiency of STAT4 and T-bet can preclude disease, suggesting that STAT4 and T-bet have important roles in both Th1 and Th17 responses. In addition,
the frequent observation of co-existence of IFN! and IL-17 producing cells in several
disease models suggest that a close relationship between Th1 and Th17 lineage.
We have developed IL-17F reporter mice that allows us to identify cells
expressing this Th17-specific cytokine. Using this model, we found that there is late
developmental plasticity of the Th17 lineage, such that IFN! producing cells emerged
from Th17 cells following lineage commitment. This transition occurred in a STAT4 and
T-bet dependent manner. We also examined the potential consequence of this shift for
immunopathology. In a parallel with Th1, we observed that IL-23 acts synergistically
with IL-1 or IL-18 to induce unique cytokines of the Th17 lineage in Th17 cells,
independently of T cell receptor (TCR) stimulation. Moreover, Th17 cells respond to IL-
18 plus IL-12 to induce IFN! expression that supports late Th17 developmental plasticity.
Our results suggest that Th17 effector development is programmed for late
developmental plasticity and that non-antigen-specific responses may enhance the role of
Th17 cells in autoimmunity and host protection.
1 online resource (x, 139 p. : ill., digital, PDF file)
Microbiology;
Joint Health Sciences;
Th17
IL-17
UNRESTRICTED
Advisors/Committee Members: Weaver, Casey T., Benveniste, Tika<br>, Chaplin, David D.<br>, Elson, Charles O.<br>, Klug, Christopher A..
Subjects/Keywords: Cell Lineage – immunology<; br>;
Interleukin-17 – metabolism<; br>;
T-Lymphocyte Subsets – immunology<; br>;
Th1 Cells – immunology<; br>;
Th2 Cells – immunology<; br>;
Transforming Growth Factor beta – metabolism
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APA (6th Edition):
Lee, Y. K. (2009). Late developmental plasticity in the T helper 17 lineage. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,916
Chicago Manual of Style (16th Edition):
Lee, Yun Kyung. “Late developmental plasticity in the T helper 17 lineage.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,916.
MLA Handbook (7th Edition):
Lee, Yun Kyung. “Late developmental plasticity in the T helper 17 lineage.” 2009. Web. 12 Dec 2019.
Vancouver:
Lee YK. Late developmental plasticity in the T helper 17 lineage. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,916.
Council of Science Editors:
Lee YK. Late developmental plasticity in the T helper 17 lineage. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,916
21.
윤, 영실.
Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구.
Degree: 2005, Ajou University
URL: http://repository.ajou.ac.kr/handle/201003/2293
;
http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229
► "목적: 모든 정상 세포는 제한된 수의 분열을 거친 후 더 이상 분열하지 않는 “replicative senescence”라는 노화과정을 겪게 된다. 세포노화의 원인으로 “free radical theory”가 잘 알려져…
(more)
▼ "목적: 모든 정상 세포는 제한된 수의 분열을 거친 후 더 이상 분열하지 않는 “replicative senescence”라는 노화과정을 겪게 된다. 세포노화의 원인으로 “free radical theory”가 잘 알려져 있으나, 최근 연구에서는 미토콘드리아가 세포 내 활성산소 발생의 주 원인일 뿐 아니라 그 자체가 활성산소에 의해 손상을 받을 수 있다는 것을 고려하여 mitochondria의 손상이 노화의 원인이 될 것이라는 “mitochondrial DNA hypothesis”가 제시되고 있다. 상피세포의 성장을 억제하는 것으로 잘 알려진 Transforming Growth Factor β1 (TGF β1)가 최근에는 세포노화과정에도 관여하고 있다는 결과들이 보고되었다. 그러나 자세한 생화학적 기전에 대해서는 연구가 전무하다. 따라서 이 연구에서는 TGF β1이 mink lung epithelial cells에서 세포노화를 야기할 수 있는지, 이 때 미토콘드리아의 손상이 어떻게 관여하고 있는지를 조사하고자 한다.
재료 및 방법 방법: Mv1Lu mink lung epithelial cells에 TGF β1을 처리하고 세포 내 여러 변화들을 관찰하였다. Cell cycle, ROS generation, 그리고 mitochondrial membrane potential 등은 flow cytometry 방법으로 측정하였다. 미토콘드리아의 respiratory complex의 활성은 spectrophotometry 방법과 세포의 호흡률 조사를 통해 분석하였다. 단백질의 발현 양상은 immunocytochemistry와 immunoblotting을 통해 조사하였다. 미토콘드리아의 형태는 전자현미경을 이용하여 관찰하였다.
결과: Mv1Lu cells에 10 % serum 조건에서 TGF β1을 처리하였을 때 cell cycle이 G1 phase에 arrest 되면서 세포가 senescent phenotype을 나타내었으나, 5% 이하의 낮은 serum 농도에서는 apoptosis가 유도되었다. 이런 arrest과정 동안 지속적으로 ROS가 생성되고 mitochondrial membrane potential (ΔΨm)이 감소되었다. 따라서, mitochondrial defect와 ROS production간에 어떤 상관관계가 있는지에 대해 조사하였다. Mv1Lu cells에 antioxidant를 전처리 하였을 때 ROS의 생성은 효과적으로 억제되었으나 ΔΨm의 disruption은 억제하지 못했고, KCN이나 oligomycin으로 mitochondrial respiratory chain의 기능을 완전히 저해하였을 때 ROS의 생성도 완전히 억제되었다. 게다가, TGF β1에 의해 mitochondria 의 complex Ⅳ activity가 감소되고 그것에 의해 respiration rate도 점차 감소되었다. 이런 결과들로 볼 때, complex Ⅳ activity의 감소로 인한 mitochondrial respiratory defect가 지속적인 ROS 생성의 원인임을 알 수 있었다. 또한 mitochondria에 존재하는 PrxⅢ가 oxidation되는 것을 보아 respiratory defect가 mitochondrial oxidative stress를 유발함을 알 수 있다. 마지막으로, hepatocyte growth factor는 mitochondrial respiration의 defect를 억제하고, 그에 따라 ΔΨm disruption 과 ROS generation을 저해함으로써 Mv1Lu cells이 TGF β1에 의한 senescence-like growth arrest현상을 나타내지 않게 하였다.
결론: 이 연구의 결과에서, TGF β1은 5 % 이상의 serum 조건에서 Mv1Lu cell의 senescence-like growth arrest를 유도하였다. Arrest 과정 동안 mitochondria의 complex activity Ⅳ 의 감소로 인한 respiration의 defect로 인해 ROS가 지속적으로 생성되었다. 또한 HGF는 mitochondrial dysfunction을 막아서 세포가 arrest되지 않게 하였다. 이들 결과들은 mitochondrial defect가 또한 single cytokine인 TGF β1에 의해 유도되는 senescence 과정에 관여하고 있음을 보여준다. 따라서 이들 결과는 aging에서의 ‘mitochondrial theory’가 중요함을 의미하고 TGF β1-induced signaling과 mitochondrial metabolism의 조절기전 사이에 중요한 상관관계가 있음을 보여준다."
"Purpose:Normal cells enter a nondividing state after a finite number of population doubling, which is termed replicative senescence. Although the free radical theory has long been implicated in the senescence, recent studies have emphasized mitochondrial DNA hypothesis because mitochondria is the major ROS generator in addition to its high vulnerability to oxidative damage. Transforming growth factor β1 (TGF β1) has well been known to suppress epithelial cell growth and recently been described to be involved in cellular senescence. The purpose of this study is to investigate how TGF β1 could induce senescence in Mv1Lu mink lung epithelial cells, whether and how mitochondrial defects are involved in the senescence.
Materials and Methods: Mink…
Advisors/Committee Members: 200224342, 윤, 영실.
Subjects/Keywords: Transforming Growth Factor beta1 (TGF β1); senescence-like growth arrest; mitochondrial dysfunction; Reactive Oxygen Species (ROS); cellular respiration; Hepatocyte Growth Factor (HGF)
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APA ·
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APA (6th Edition):
윤, . (2005). Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229
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):
윤, 영실. “Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구.” 2005. Thesis, Ajou University. Accessed December 12, 2019.
http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
윤, 영실. “Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구.” 2005. Web. 12 Dec 2019.
Vancouver:
윤 . Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구. [Internet] [Thesis]. Ajou University; 2005. [cited 2019 Dec 12].
Available from: http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
윤 . Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구. [Thesis]. Ajou University; 2005. Available from: http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université de Montréal
22.
Grégoire, Catherine-Alexandra.
Mechanisms underlying activation of neural stem cells in the adult central nervous system
.
Degree: 2016, Université de Montréal
URL: http://hdl.handle.net/1866/15972
► À la fin du 19e siècle, Dr. Ramón y Cajal, un pionnier scientifique, a découvert les éléments cellulaires individuels, appelés neurones, composant le système nerveux.…
(more)
▼ À la fin du 19e siècle, Dr. Ramón y Cajal, un pionnier scientifique, a découvert les
éléments cellulaires individuels, appelés neurones, composant le système nerveux. Il a
également remarqué la complexité de ce système et a mentionné l’impossibilité de ces nouveaux
neurones à être intégrés dans le système nerveux adulte. Une de ses citations reconnues : “Dans
les centres adultes, les chemins nerveux sont fixes, terminés, immuables. Tout doit mourir, rien
ne peut être régénérer” est représentative du dogme de l’époque (Ramón y Cajal 1928).
D’importantes études effectuées dans les années 1960-1970 suggèrent un point de vue différent.
Il a été démontré que les nouveaux neurones peuvent être générés à l’âge adulte, mais cette
découverte a créé un scepticisme omniprésent au sein de la communauté scientifique. Il a fallu
30 ans pour que le concept de neurogenèse adulte soit largement accepté. Cette découverte, en
plus de nombreuses avancées techniques, a ouvert la porte à de nouvelles cibles thérapeutiques
potentielles pour les maladies neurodégénératives. Les cellules souches neurales (CSNs) adultes
résident principalement dans deux niches du cerveau : la zone sous-ventriculaire des ventricules
latéraux et le gyrus dentelé de l’hippocampe. En condition physiologique, le niveau de
neurogenèse est relativement élevé dans la zone sous-ventriculaire contrairement à
l’hippocampe où certaines étapes sont limitantes. En revanche, la moelle épinière est plutôt
définie comme un environnement en quiescence.
Une des principales questions qui a été soulevée suite à ces découvertes est : comment
peut-on activer les CSNs adultes afin d’augmenter les niveaux de neurogenèse ? Dans
l’hippocampe, la capacité de l’environnement enrichi (incluant la stimulation cognitive,
l’exercice et les interactions sociales) à promouvoir la neurogenèse hippocampale a déjà été
démontrée. La plasticité de cette région est importante, car elle peut jouer un rôle clé dans la
récupération de déficits au niveau de la mémoire et l’apprentissage. Dans la moelle épinière, des
études effectuées in vitro ont démontré que les cellules épendymaires situées autour du canal
central ont des capacités d’auto-renouvellement et de multipotence (neurones, astrocytes,
oligodendrocytes). Il est intéressant de noter qu’in vivo, suite à une lésion de la moelle épinière,
les cellules épendymaires sont activées, peuvent s’auto-renouveller, mais peuvent seulement
ii
donner naissance à des cellules de type gliale (astrocytes et oligodendrocytes). Cette nouvelle
fonction post-lésion démontre que la plasticité est encore possible dans un environnement en
quiescence et peut être exploité afin de développer des stratégies de réparation endogènes dans
la moelle épinière.
Les CSNs adultes jouent un rôle important dans le maintien des fonctions physiologiques
du cerveau sain et dans la réparation neuronale suite à une lésion. Cependant, il y a peu de
données sur les mécanismes qui permettent l'activation des CSNs en quiescence permettant de
maintenir ces…
Advisors/Committee Members: Fernandes, Karl J.L (advisor).
Subjects/Keywords: cellules souches neurales;
neurogenèse adulte;
hippocampe;
moelle épinière;
environnement enrichi;
exercice;
comportement;
neuroinflammation;
transforming growth factor-beta1;
cellules initiatrices de neurosphères;
neural stem cells;
adult neurogenesis;
hippocampus;
spinal cord;
environmental enrichment;
exercise;
behaviour;
neurosphere-initiating cells
Record Details
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APA ·
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MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Grégoire, C. (2016). Mechanisms underlying activation of neural stem cells in the adult central nervous system
. (Thesis). Université de Montréal. Retrieved from http://hdl.handle.net/1866/15972
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):
Grégoire, Catherine-Alexandra. “Mechanisms underlying activation of neural stem cells in the adult central nervous system
.” 2016. Thesis, Université de Montréal. Accessed December 12, 2019.
http://hdl.handle.net/1866/15972.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Grégoire, Catherine-Alexandra. “Mechanisms underlying activation of neural stem cells in the adult central nervous system
.” 2016. Web. 12 Dec 2019.
Vancouver:
Grégoire C. Mechanisms underlying activation of neural stem cells in the adult central nervous system
. [Internet] [Thesis]. Université de Montréal; 2016. [cited 2019 Dec 12].
Available from: http://hdl.handle.net/1866/15972.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Grégoire C. Mechanisms underlying activation of neural stem cells in the adult central nervous system
. [Thesis]. Université de Montréal; 2016. Available from: http://hdl.handle.net/1866/15972
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
23.
Tanner, Scott.
Regulatory T Cells In The Fvb.mdr1a-/- Model Of Colitis.
Degree: 2012, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,1795
► Regulatory T cells (Treg) are necessary for the maintenance of immune homeostasis, and have been implicated in several autoimmune diseases, including inflammatory bowel disease (IBD).…
(more)
▼ Regulatory T cells (Treg) are necessary for the maintenance of immune homeostasis, and have been implicated in several autoimmune diseases, including inflammatory bowel disease (IBD). Most murine studies focusing on the function of Tregs have been done on the C57BL/6 or BALB/c background, creating a bias towards these two strains. In addition, it has been shown that C57BL/6 and BALB/c Tregs function in different manners. To further investigate potential strain differences in Treg phenotype and function, we chose to analyze FVB/N Tregs. Several differences were observed, including de-creased FVB/N Treg suppression in a non-cell contact dependent manner, decreased FVB/N and BALB/c Treg surface expression of glycoprotein A repetitions predominant (GARP) and latency associated peptide (LAP) and decreased <italic>Cste</italic> mRNA expression on C57BL/6 Tregs. In addition, BALB/c natural Tregs (nTregs) were more capable of main-taining Foxp3 expression, and C57BL/6 CD4<super>+</super>CD25<super>-</super> naïve T cells were more likely to be induced to express Foxp3 when exposed to TGF-β and to become induced Tregs (iTregs). These data suggest there are genetic differences between the phentoype and function of Treg cells that should be taken into account in future Treg studies. The FVB.<italic>mdr1a</italic><super>-/-</super> mouse, lacking the small molecule pump P-glycoprotein (P-gp), develops spontaneous T cell mediated colitis. In addition, <italic>MDR1</italic> polymorphisms and P-gp deficiency in humans have been linked to the development of ulcerative colitis. We chose this model to investigate the role of Tregs in IBD development. Our studies demonstrated a significant decrease of Foxp3<super>+</super> Tregs in the Peyer's patches and small in-testinal lamina propria of FVB.<italic>mdr1a</italic><super>-/-</super> mice, which precedes spontaneous disease in these animals. We did not observe altered trafficking, apoptosis, or plasticity of FVB.<italic>mdr1a</italic><super>-/-</super> Tregs. However, FVB.<italic>mdr1a</italic><super>-/-</super> mice were unable to generate iTregs effectively, both <italic>in vitro</italic> and <italic>in vivo</italic>. Without the generation of iTregs, FVB.<italic>mdr1a</italic><super>-/-</super> animals are more susceptible to intestinal inflammation. In concordance with our studies, the susceptibility of FVB.<italic>mdr1a</italic><super>-/-</super> mice to colonic inflammation may influence the difference in Treg function between the two strains. The presence of the <italic>MDR1</italic> polymorphism in the human population demonstrates the importance of understanding the function of Tregs in the IBD patient population.
PhD
1 online resource (x, 135 pages) :illustrations
Ph.D.University of Alabama at…
Advisors/Committee Members: Robin G. Lorenz, Elson, Charles O. Ponnazhagan,Selvarangan Smythies, Lesley E. Steele,Chad.
Subjects/Keywords: Colitis – immunology.<; br>; Intestines – immunology<; br>; P-Glycoproteins<; br>; T-Lymphocytes, Regulatory – immunology<; br>; Transforming Growth Factor beta – pharmacology
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APA ·
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to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Tanner, S. (2012). Regulatory T Cells In The Fvb.mdr1a-/- Model Of Colitis. (Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1795
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):
Tanner, Scott. “Regulatory T Cells In The Fvb.mdr1a-/- Model Of Colitis.” 2012. Thesis, University of Alabama – Birmingham. Accessed December 12, 2019.
http://contentdm.mhsl.uab.edu/u?/etd,1795.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Tanner, Scott. “Regulatory T Cells In The Fvb.mdr1a-/- Model Of Colitis.” 2012. Web. 12 Dec 2019.
Vancouver:
Tanner S. Regulatory T Cells In The Fvb.mdr1a-/- Model Of Colitis. [Internet] [Thesis]. University of Alabama – Birmingham; 2012. [cited 2019 Dec 12].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,1795.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Tanner S. Regulatory T Cells In The Fvb.mdr1a-/- Model Of Colitis. [Thesis]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1795
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
24.
정, 수령.
hepatocyte growth factor inhibits glial scar formation and.
Degree: 2009, Ajou University
URL: http://repository.ajou.ac.kr/handle/201003/2272
;
http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010119
► Formation of glial scars physically impedes growth of regenerating axons following CNS injuries such as spinal cord trauma. Glial scars also produce various species of…
(more)
▼ Formation of glial scars physically impedes growth of regenerating axons following CNS injuries such as spinal cord trauma. Glial scars also produce various species of chondroitin sulfate proteoglycans (CSPGs) that act as a potent inhibitor of axon growth. Thus, inhibition of glial scar formation and/or suppression of CSPGs production may support axonal regeneration following spinal cord injury. Hepatocyte growth factor (HGF), which was originally identified as a mitogen for hepatocytes, has been shown to strongly suppress fibrosis of internal organs such as liver and kidney. However, its role in the regulation of CNS glial scars has not been studied. The purpose of this study was to examine whether HGF can affect formation of glial scars and production of various CSPGs. Glial scar formation was mimicked in vitro by cytokine treatment in primary astrocyte culture. Treatment of TGFβ1 led to astrocytic hypertrophy that was associated with dramatic upregulation of intermediate filament, GFAP (glial fibrillary acidic protein), which was evidently suppressed by HGF cotreatment in a dose-dependent manner. HGF also inhibited TGFβ1-induced upregulation of neurocan, one of CSPG species. To explore whether glial scar formation is inhibited by HGF in vivo spinal cord injury model, HGF overexpressing mesenchymal stem cells (HGF-MSCs) were transplanted into hemisected spinal cord lesions at T8. The ex-vivo gene delivery approach effectively increased the HGF level and phosphorylation of its cognate receptor c-Met. Transplantation of HGF-MSCs reduced the formation glial scar and CSPGs deposition around the hemisection lesions. Western blot showed that the amount of neurocan significantly decreased in animals with HGF-MSCs transplantation. These findings were accompanied by decreases in TGFβ1 and β2, strong inducers of astrocyte activation. Our results suggest that HGF may potently regulate both glial scar formation and CSPGs production following spinal cord injury
"ABSTRACT ⅰ
TABLE OF CONTENTS ⅲ
LIST OF FIGURES ⅴ
LIST OF TABLE ⅵ
LIST OF ABBREVIATION ⅶ
Ⅰ. INTRODUCTION 1
Ⅱ. MATERIAL AND METHODS 5
A. PRIMARY ASTROCYTE CULTURES 5
B. ANIMALS AND SURGICAL PROCEDURES 6
C. IMMUNOCYTOCHEMISTRY 7
D. TISSUE PROCESSING AND IMMUNOHISTOCHEMISTRY 7
E. ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA) 8
F. WESTERN BLOT ANALYSIS 9
G. REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION (RT-PCR) 11
H. STASTITATIC ANALYSIS 12
Ⅲ. RESULTS 13
A. HGF prevents cytokine-induced astrocytic activation in vitro. 13
B. HGF decreases expression of chondroitin sulfate proteoglycans (CSPGs) 19
C. Effects of HGF on TGFβ secretion 22
D. Ex vivo delivery of HGF using mesenchymal stem cells in hemisection spinal cord injury. 27
E. HGF inhibits astrocytic activation and CSPGs production after spinal cord injury. 33
Ⅳ. DISCUSSION 38
Ⅴ. CONCLUSION 43
REFERENCE 44
국문요약 55
"
Master
Advisors/Committee Members: 200724510, 정, 수령.
Subjects/Keywords: spinal cord injury; hepatocyte growth factor; glial scars; chondroitin sulfate proteoglycans; transforming growth factor
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Manager
APA (6th Edition):
정, . (2009). hepatocyte growth factor inhibits glial scar formation and. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/2272 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010119
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):
정, 수령. “hepatocyte growth factor inhibits glial scar formation and.” 2009. Thesis, Ajou University. Accessed December 12, 2019.
http://repository.ajou.ac.kr/handle/201003/2272 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010119.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
정, 수령. “hepatocyte growth factor inhibits glial scar formation and.” 2009. Web. 12 Dec 2019.
Vancouver:
정 . hepatocyte growth factor inhibits glial scar formation and. [Internet] [Thesis]. Ajou University; 2009. [cited 2019 Dec 12].
Available from: http://repository.ajou.ac.kr/handle/201003/2272 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010119.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
정 . hepatocyte growth factor inhibits glial scar formation and. [Thesis]. Ajou University; 2009. Available from: http://repository.ajou.ac.kr/handle/201003/2272 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000010119
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Florida International University
25.
Stewart, Tiffanie S.
Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population.
Degree: PhD, Dietetics and Nutrition, 2016, Florida International University
URL: http://digitalcommons.fiu.edu/etd/2459
;
10.25148/etd.FIDC000286
;
FIDC000286
► Liver disease is now a leading cause of non-AIDS related morbidity and mortality in people living with HIV (PLWH). The present study investigated the…
(more)
▼ Liver disease is now a leading cause of non-AIDS related morbidity and mortality in people living with HIV (PLWH). The present study investigated the interplay between adverse lifestyle factors that are prevalent in PLWH, biological mediators of liver pathogenesis, and a non-invasive measure of liver fibrosis (FIB-4 index) in HIV mono- and HIV/HCV co-infected individuals.
The results of this investigation in the Miami Adult Studies of HIV (MASH) cohort show that the odds of liver fibrosis progression significantly increased over two years for HIV mono-infected participants who drank alcohol hazardously (OR 3.038,
P=0.048), and had BMI ≥ 28kg/m
2 (OR 2.934,
P=0.027). Cocaine use reduced the odds of advancing one stage of liver fibrosis (OR 0.228,
P=0.038), but an interaction between high BMI and cocaine use slightly raised the odds by 4.8% of liver fibrosis progression (
P=0.072). HIV/HCV co-infected participants showed interactions between cocaine use and high BMI with increased FIB-4 stage (OR 4.985,
P= 0.034), however no lifestyle factors could independently predict FIB-4 stage in this group.
Biological mediators previously associated with liver pathogenesis were associated with higher FIB-4 index over 2 years in a subset of (n=65) HIV mono-infected participants. Plasma measures of oxidative stress (% oxidized glutathione: OR 4.342,
P= 0.046), hepatocyte-specific apoptosis (Cytokeratin-18 (CK-18): OR 1.008,
P=0.021), and microbial endotoxin (lipopolysaccharide (LPS): OR 1.098,
P= 0.097) were associated with having higher odds of progressing at least one stage of FIB-4 over 2 years.
The same biological mediators were also associated with liver fibrosis within HIV infected people who also had a harmful lifestyle characteristic. FIB-4 index was significantly associated with % oxidized glutathione in obese subjects (β=0.563,
P=0.018), TGF-β1 in cocaine users (β=0.858,
P=0.027), and CK-18 in HIV infected individuals without any adverse lifestyle factors (β=0.435,
P=0.015).
Taken together, the findings of these studies describe interrelationships between HIV disease status, lifestyle, and biological mediators of liver fibrosis. The results show interactions between lifestyle conditions and the mediators of liver fibrosis may account for higher rates of liver disease in HIV infection. Research is warranted to develop personalized therapeutics for PLWH to curb the burden of liver disease.
Advisors/Committee Members: Adriana Campa, Fatma Huffman, Marianna Baum, Juan Liuzzi, Wensong Wu.
Subjects/Keywords: HIV infection; HIV/HCV co-infection; liver fibrosis; alcohol; AUDIT; cocaine; body mass index; FIB-4 index; oxidative stress; hepatocyte apoptosis; transforming growth factor-beta1; microbial endotoxin; malondialdehyde; glutathione; MDA; GSH; TGF-β1; CK-18; LPS; Biochemical Phenomena, Metabolism, and Nutrition; Community Health and Preventive Medicine; Dietetics and Clinical Nutrition; Hepatology; Medical Biochemistry; Medical Immunology; Medical Nutrition; Other Medical Sciences
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MLA ·
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CSE |
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APA (6th Edition):
Stewart, T. S. (2016). Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population. (Doctoral Dissertation). Florida International University. Retrieved from http://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286
Chicago Manual of Style (16th Edition):
Stewart, Tiffanie S. “Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population.” 2016. Doctoral Dissertation, Florida International University. Accessed December 12, 2019.
http://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286.
MLA Handbook (7th Edition):
Stewart, Tiffanie S. “Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population.” 2016. Web. 12 Dec 2019.
Vancouver:
Stewart TS. Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population. [Internet] [Doctoral dissertation]. Florida International University; 2016. [cited 2019 Dec 12].
Available from: http://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286.
Council of Science Editors:
Stewart TS. Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population. [Doctoral Dissertation]. Florida International University; 2016. Available from: http://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286
26.
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki.
Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.
Degree: 博士（歯学）, 2014, Fukuoka Dental College / 福岡歯科大学
URL: http://id.nii.ac.jp/1167/00000003/
► Transforming growth factor-β1 (TGF-β1) reportedly causes the differentiation of fibroblasts to myofibroblasts during wound healing. We investigated the mechanism underlying the activation of latent TGF-β1…
(more)
▼ Transforming growth factor-β1 (TGF-β1) reportedly causes the differentiation of fibroblasts to myofibroblasts during wound healing. We investigated the mechanism underlying the activation of latent TGF-β1 released by keratinocytes in efforts to identify promising pharmacological approaches for the prevention of hypertrophic scar formation. A three-dimensional collagen gel matrix culture was prepared using rat keratinocytes and dermal fibroblasts. Stratified keratinocytes promoted the TGF receptor-dependent increase in α-smooth muscle actin (α-SMA) immunostaining and mRNA levels in fibroblasts. Latent TGF-β1 was found to be localized suprabasally and secreted. α-SMA expression was inhibited by an anti-αv-integrin antibody and a matrix metalloproteinase (MMP) inhibitor, GM6001. In a two-dimensional fibroblast culture, α-SMA expression depended on the production of endogenous TGF-β1 and required αv-integrin or MMP for the response to recombinant latent TGF-β1. In keratinocyte-conditioned medium, MMP-dependent latent TGF-β1 secretion was detected. Applying this medium to the fibroblast culture enhanced α-SMA production. This effect was decreased by GM6001, the anti-αv-integrin antibody, or the preabsorption of latent TGF-β1. These results indicate that keratinocytes secrete latent TGF-β1, which is liberated to fibroblasts over distance and is activated to produce α-SMA with the aid of a positive-feedback loop. MMP inhibition was effective for targeting both keratinocytes and fibroblasts in this model.
2013年度
Subjects/Keywords: keratinocyte; fibroblast; transforming growth factor-β1; αv-integrin; matrix metalloproteinase
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APA (6th Edition):
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, H. (2014). Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000003/
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):
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. “Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.” 2014. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed December 12, 2019.
http://id.nii.ac.jp/1167/00000003/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. “Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.” 2014. Web. 12 Dec 2019.
Vancouver:
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa H. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. [cited 2019 Dec 12].
Available from: http://id.nii.ac.jp/1167/00000003/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa H. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. Available from: http://id.nii.ac.jp/1167/00000003/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
27.
Wu, Wei-Hao.
The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats.
Degree: Master, Marine Biotechnology and Resources, 2013, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809
► Diabetes mellitus is a metabolic disease that can have long-term complications, including diabetic neuropathy pain. Base on preliminary screening, we had found that a marine-derived…
(more)
▼ Diabetes mellitus is a metabolic disease that can have long-term complications, including diabetic neuropathy pain. Base on preliminary screening, we had found that a marine-derived compound, SWV-1 has potential in vitro anti-inflammatory effects. In present study, we found that intrathecal or oral SWV-1 produce antinociceptive effects in STZ-induced diabetic neuropathic rats. Moreover, compare with ziconotide, SWV-1 did not produced any obvious adverse effects. Immunohistochemistical analyses also showed that SWV-1 significantly attenuated STZ-induced spinal neuroninflammation. We further demonstrated that administration of TGF-β type I receptor inhibitor attenuate the analgesic effect of SWV-1 in STZ-rats. In conclusion, SWV-1 is a potential candidate compound for drug development to treat neuropathic pain in patients with diabetes.
Advisors/Committee Members: Zhi-Hong Wen (committee member), San-Nan Yang (chair), Jyh-Yih Chen (chair).
Subjects/Keywords: neuroinflammation; immunohistochemistry; transforming growth factor-β; antinociceptive effects
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APA ·
Chicago ·
MLA ·
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CSE |
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APA (6th Edition):
Wu, W. (2013). The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809
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):
Wu, Wei-Hao. “The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats.” 2013. Thesis, NSYSU. Accessed December 12, 2019.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wu, Wei-Hao. “The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats.” 2013. Web. 12 Dec 2019.
Vancouver:
Wu W. The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats. [Internet] [Thesis]. NSYSU; 2013. [cited 2019 Dec 12].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wu W. The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats. [Thesis]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
28.
Chen, Zhi-Cheng.
The effects of skeleton extract obtained from marine organisms on wound healing.
Degree: PhD, Marine Biotechnology and Resources, 2017, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748
► Shijueming (SJM) is a traditional Chinese medicine. Records from 1757, in the Qing dynasty, detail the use of SJM for treating skin injuries, particularly poorly…
(more)
▼ Shijueming (SJM) is a traditional Chinese medicine. Records from 1757, in the Qing dynasty, detail the use of SJM for treating skin injuries, particularly poorly managed ulcers or traumatic wounds. However, no study has yet adopted an animal model to verify the phenomenon described in these records regarding the efficacy of SJM in promoting wound healing. In studies identifying novel bioactive materials in natural products that are useful for treating skin injuries, os sepiae (OS) extract has been reported to have a wound-healing effect. Therefore, this study used in vitro and in vivo models and performed tissue section analysis and Western blotting to evaluate the effect of SJM and OS on wound healing. RAW264.7 cells were used in antiinflammatory activity and phagocytic assays. Male Wistar rats were used to evaluate the effect of SJM and OS on burn and excision wound healing. The results were analyzed through hematoxylin and eosin staining, picrosirius red staining, and Western blotting. The results revealed that in the in vitro model, SJM promoted the phagocytic activity of RAW264.7 cells and OS promoted EA. hy 926 endothelial cell migration. Both SJM and OS reduced inducible nitric oxide synthase (iNOS) expression and enhanced macrophage phagocytosis in vitro. Compared with vehicle-treated rats, both SJM and OS significantly promoted wound healing in the rat burn injury model. Furthermore, SJM reduced neutrophil infiltration and promoted
transforming growth factor-beta 1 (TGF-β1) protein expression, thus increasing the collagen I content. We suggest that the mechanism through which SJM and OS promote wound healing is related to macrophage activation and angiogenesis enhancement, respectively. In the inflammatory phase, both SJM and OS alleviate inflammation by inhibiting iNOS expression and removing neutrophils through phagocytosis. Furthermore, SJM induces TGF-β1 secretion, converting collagen during the tissue remodeling phase. These findings indicate that SJM is a promising therapeutic option for treating burn injury.
Advisors/Committee Members: Ming-Hong Tai (chair), Wen-Sheng Liu (chair), Hui-Min Wang (chair), Zhi-Hong Wen (committee member), Hsiu-Chin Lin (chair), Yao-Chang Chen (chair), Chien-Chih Chiu (chair).
Subjects/Keywords: wound healing; Shijueming; os sepiae; macrophage; transforming growth factor-beta
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chen, Z. (2017). The effects of skeleton extract obtained from marine organisms on wound healing. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748
Chicago Manual of Style (16th Edition):
Chen, Zhi-Cheng. “The effects of skeleton extract obtained from marine organisms on wound healing.” 2017. Doctoral Dissertation, NSYSU. Accessed December 12, 2019.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748.
MLA Handbook (7th Edition):
Chen, Zhi-Cheng. “The effects of skeleton extract obtained from marine organisms on wound healing.” 2017. Web. 12 Dec 2019.
Vancouver:
Chen Z. The effects of skeleton extract obtained from marine organisms on wound healing. [Internet] [Doctoral dissertation]. NSYSU; 2017. [cited 2019 Dec 12].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748.
Council of Science Editors:
Chen Z. The effects of skeleton extract obtained from marine organisms on wound healing. [Doctoral Dissertation]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748
Ruhr Universität Bochum
29.
Beck, Lars Hendrik.
Bestimmung der Frequenz TGF-β-produzierender
T-Lymphozyten gesunder Kinder verschiedener
Altersklassen.
Degree: 2009, Ruhr Universität Bochum
URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629
► Problem: Um detailliertere Einblicke in die regelrechte Entwicklung regulatorisch bedeutsamer Immunkomponenten gewinnen zu können, wurde hier erstmals die Frequenz und der Charakter TGF-β-produzierender T-Lymphozyten gesunder…
(more)
▼ Problem: Um detailliertere Einblicke in die
regelrechte Entwicklung regulatorisch bedeutsamer Immunkomponenten
gewinnen zu können, wurde hier erstmals die Frequenz und der
Charakter TGF-β-produzierender T-Lymphozyten gesunder Kinder
verschiedener Altersklassen analysiert. Methode: Es wurden
durchflusszytometrische Analysen stimulierter
T-Zell-Subpopulationen venöser Blutproben von über 100 gesunden
Kindern verschiedener Altersklassen durchgeführt. Ergebnis: Die
Ergebnisse der vorliegenden Studie demonstrieren erstmalig eine mit
dem Alter wachsende Kompetenz des T- lymphozytären Systems zur
Produktion des löslichen Zytokins TGF-β. Es existierten keine
Hinweise auf eine hervorstechende TGF-β-Synthesekapazität im
Kompartiment der reifen CD4pos-CD25pos-CD45RAneg-regulatorischen
T-Zellen. Diskussion: Der wachsende Anteil TGF-β-produzierender
Zellen wird von uns als Ausdruck der Reifung im Sinne der
funktionellen Entwicklung effizienter T-Zell-Klone
interpretiert.
Advisors/Committee Members: Medizin.
Subjects/Keywords: Transforming Growth Factor beta; T-Lymphozyt;
Helferzelle; Immunologie
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Beck, L. H. (2009). Bestimmung der Frequenz TGF-β-produzierender
T-Lymphozyten gesunder Kinder verschiedener
Altersklassen. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629
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):
Beck, Lars Hendrik. “Bestimmung der Frequenz TGF-β-produzierender
T-Lymphozyten gesunder Kinder verschiedener
Altersklassen.” 2009. Thesis, Ruhr Universität Bochum. Accessed December 12, 2019.
http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Beck, Lars Hendrik. “Bestimmung der Frequenz TGF-β-produzierender
T-Lymphozyten gesunder Kinder verschiedener
Altersklassen.” 2009. Web. 12 Dec 2019.
Vancouver:
Beck LH. Bestimmung der Frequenz TGF-β-produzierender
T-Lymphozyten gesunder Kinder verschiedener
Altersklassen. [Internet] [Thesis]. Ruhr Universität Bochum; 2009. [cited 2019 Dec 12].
Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Beck LH. Bestimmung der Frequenz TGF-β-produzierender
T-Lymphozyten gesunder Kinder verschiedener
Altersklassen. [Thesis]. Ruhr Universität Bochum; 2009. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Ruhr Universität Bochum
30.
Pennartz, Christian.
Untersuchungen zur Modulation der intestinalen
Epithelrestitution in vitro durch Vascular endothelian growth
factor.
Degree: 2009, Ruhr Universität Bochum
URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034
► Chronisch entzündliche Darmerkrankungen sind geprägt durch destruierende Entzündungs-reaktionen der Darmschleimhaut. Bei intakter Basalmembran werden kleinere Epitheldefekte mittels der Epithelzellrestitution unabhängig von der Proliferation repariert. Ziel…
(more)
▼ Chronisch entzündliche Darmerkrankungen sind
geprägt durch destruierende Entzündungs-reaktionen der
Darmschleimhaut. Bei intakter Basalmembran werden kleinere
Epitheldefekte mittels der Epithelzellrestitution unabhängig von
der Proliferation repariert. Ziel dieser Arbeit war es, die Rolle
von VEGF bei der intestinalen Epithelzellrestitution mit Hilfe
eines in vitro Wundheilungsmodells zu analysieren. Konfluente
Caco-2- und IEC-18-Monolayer wurden hierfür verletzt und mit VEGF
inkubiert. Die Zellmigration wurde durch die Anzahl der über den
Wundrand gewanderten Zellen bestimmt. Die Proliferation wurde
mittels MTT-Test bestimmt. Resultierend steigert VEGF signifikant
die Migration von Caco-2- und IEC-18-Zellen. Dieser Effekt lässt
sich durch den TGF-β-Antikörper aufheben. Die Proliferation wird
durch VEGF nicht signifikant erhöht. VEGF führt in vitro somit zur
einer TGF-β-abhängigen signifikanten Verbesserung der
Epithelzellrestitution bei Caco-2- und
IEC-18-Zellen.
Advisors/Committee Members: Medizin.
Subjects/Keywords: Migration (Biologie); Proliferation; Transforming
Growth Factor beta; Chronische Darmentzündung
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APA ·
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MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
Pennartz, C. (2009). Untersuchungen zur Modulation der intestinalen
Epithelrestitution in vitro durch Vascular endothelian growth
factor. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034
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):
Pennartz, Christian. “Untersuchungen zur Modulation der intestinalen
Epithelrestitution in vitro durch Vascular endothelian growth
factor.” 2009. Thesis, Ruhr Universität Bochum. Accessed December 12, 2019.
http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Pennartz, Christian. “Untersuchungen zur Modulation der intestinalen
Epithelrestitution in vitro durch Vascular endothelian growth
factor.” 2009. Web. 12 Dec 2019.
Vancouver:
Pennartz C. Untersuchungen zur Modulation der intestinalen
Epithelrestitution in vitro durch Vascular endothelian growth
factor. [Internet] [Thesis]. Ruhr Universität Bochum; 2009. [cited 2019 Dec 12].
Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Pennartz C. Untersuchungen zur Modulation der intestinalen
Epithelrestitution in vitro durch Vascular endothelian growth
factor. [Thesis]. Ruhr Universität Bochum; 2009. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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