subject:(TGFB)

University of Florida

1. Azie, Obiora Chidume. Control over Cell Signaling via Magnetic Actuation of Latent Growth Factors.

Degree: PhD, Materials Science and Engineering, 2019, University of Florida

► Conjugation of latent growth factors to superparamagnetic iron oxide nanoparticles (SPION) is potentially useful for magnetically triggered release of bioactive macromolecules. Thus, the goal of… (more)

Subjects/Keywords: conjugation – spion – tgfb

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APA (6^th Edition):

Azie, O. C. (2019). Control over Cell Signaling via Magnetic Actuation of Latent Growth Factors. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0055739

Chicago Manual of Style (16^th Edition):

Azie, Obiora Chidume. “Control over Cell Signaling via Magnetic Actuation of Latent Growth Factors.” 2019. Doctoral Dissertation, University of Florida. Accessed January 20, 2021. https://ufdc.ufl.edu/UFE0055739.

MLA Handbook (7^th Edition):

Azie, Obiora Chidume. “Control over Cell Signaling via Magnetic Actuation of Latent Growth Factors.” 2019. Web. 20 Jan 2021.

Vancouver:

Azie OC. Control over Cell Signaling via Magnetic Actuation of Latent Growth Factors. [Internet] [Doctoral dissertation]. University of Florida; 2019. [cited 2021 Jan 20]. Available from: https://ufdc.ufl.edu/UFE0055739.

Council of Science Editors:

Azie OC. Control over Cell Signaling via Magnetic Actuation of Latent Growth Factors. [Doctoral Dissertation]. University of Florida; 2019. Available from: https://ufdc.ufl.edu/UFE0055739

University of Manchester

2. Rich, Kevin Robert. The Role of Transforming Growth Factor-Beta in T-Cell Signalling.

Degree: 2016, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:301779

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Transforming Growth Factor beta (TGFβ) is a pivotal cytokine in regulating our immune responses. TGFβ exerts many effects through T-cells, which are an important cell… (more)

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Transforming Growth Factor beta (TGFβ) is a pivotal cytokine in regulating our immune responses. TGFβ exerts many effects through T-cells, which are an important cell type in fighting infection. Functionally, TGFβ can inhibit the differentiation of naïve T-cells to pro-inflammatory T helper 1 (Th1) or Th2 cells. Conversely, TGFβ can promote the development of both pro-inflammatory Th17 cells and anti-inflammatory regulatory T-cells (Tregs). Interestingly, TGFβ exists as three isoforms with varying functions that mediate a wide scope of effects on T-cells through the same signalling machinery via Smad transcription factors, typically through Smad2, Smad3 and Smad4, and TIF1γ. However, the current mechanisms for how the TGFβ isoforms and the Smad transcription factors account for such variability in T-cell function are unclear.Here, we developed a system for exploring Smad signalling dynamics within a T-cell context using Jurkat T-cells. Our data demonstrates that Smad2 and Smad3 have varying signalling dynamics to each other and between the isoforms of TGFβ. We further demonstrate that the isoforms cause a different genetic profile in T-cells to each other and mediate gene transcription in varying reliance on specific Smads. In brief, TGFβ1 appears to favour Smad2 nuclear translocation, TGFβ2 requires Smad2, Smad3 and Smad4, and TGFβ3 has a preference for Smad3 nuclear translocation. These data indicate a more intricate mechanism of TGFβ signalling in T-cells.

T-cells are important white blood cells in our body that help the immune system fight disease. These cells can cause inflammation when they attack and sometimes attack our own bodies wrongly. Specific signals communicate to T-cells and tell them how to appropriately act. I researched a signal named Transforming Growth Factor-Beta (TGFβ) that signals via other proteins named Smads. Our research identified differences between Smad family members that may contribute differently to controlling how a T-cell behaves.

Advisors/Committee Members: PASZEK, PAWEL P, Travis, Mark, Paszek, Pawel.

Subjects/Keywords: TGFb; T-cell; Smad

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APA (6^th Edition):

Rich, K. R. (2016). The Role of Transforming Growth Factor-Beta in T-Cell Signalling. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:301779

Chicago Manual of Style (16^th Edition):

Rich, Kevin Robert. “The Role of Transforming Growth Factor-Beta in T-Cell Signalling.” 2016. Doctoral Dissertation, University of Manchester. Accessed January 20, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:301779.

MLA Handbook (7^th Edition):

Rich, Kevin Robert. “The Role of Transforming Growth Factor-Beta in T-Cell Signalling.” 2016. Web. 20 Jan 2021.

Vancouver:

Rich KR. The Role of Transforming Growth Factor-Beta in T-Cell Signalling. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Jan 20]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:301779.

Council of Science Editors:

Rich KR. The Role of Transforming Growth Factor-Beta in T-Cell Signalling. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:301779

University of Manchester

3. Rich, Kevin. The role of Transforming Growth Factor-beta in T-cell signalling.

Degree: PhD, 2016, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-transforming-growth-factorbeta-in-tcell-signalling(a04e7d47-b6f7-4524-8535-29e0a5ee0d5d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771322

► Transforming Growth Factor beta (TGFβ) is a pivotal cytokine in regulating our immune responses. TGFβ exerts many effects through T-cells, which are an important cell… (more)

Subjects/Keywords: TGFb; T-cell; Smad

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rich, K. (2016). The role of Transforming Growth Factor-beta in T-cell signalling. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-transforming-growth-factorbeta-in-tcell-signalling(a04e7d47-b6f7-4524-8535-29e0a5ee0d5d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771322

Chicago Manual of Style (16^th Edition):

Rich, Kevin. “The role of Transforming Growth Factor-beta in T-cell signalling.” 2016. Doctoral Dissertation, University of Manchester. Accessed January 20, 2021. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-transforming-growth-factorbeta-in-tcell-signalling(a04e7d47-b6f7-4524-8535-29e0a5ee0d5d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771322.

MLA Handbook (7^th Edition):

Rich, Kevin. “The role of Transforming Growth Factor-beta in T-cell signalling.” 2016. Web. 20 Jan 2021.

Vancouver:

Rich K. The role of Transforming Growth Factor-beta in T-cell signalling. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Jan 20]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-transforming-growth-factorbeta-in-tcell-signalling(a04e7d47-b6f7-4524-8535-29e0a5ee0d5d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771322.

Council of Science Editors:

Rich K. The role of Transforming Growth Factor-beta in T-cell signalling. [Doctoral Dissertation]. University of Manchester; 2016. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-transforming-growth-factorbeta-in-tcell-signalling(a04e7d47-b6f7-4524-8535-29e0a5ee0d5d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771322

University of South Carolina

4. Almurshidi, Badria. Selenium, Platinum and Cerium Oxide Nanoparticles' Applications to Cancer and Fibrotic Diseases in Medicine.

Degree: PhD, Environmental Health Sciences, 2020, University of South Carolina

URL: https://scholarcommons.sc.edu/etd/5686

► Nanomedicine is a new field of science defined by the European Science Foundation as “the science and technology of diagnosing, treating, and preventing disease… (more)

▼ Nanomedicine is a new field of science defined by the European Science Foundation as “the science and technology of diagnosing, treating, and preventing disease and traumatic injury, of relieving pain, and of preserving and improving human health, using molecular tools and molecular knowledge of the human body” (ESF 2004). The medical community has, however, made significant steps forward in understanding the potential nanomaterials may have in medical treatment of certain diseases. Current nanoparticles being evaluated include platinum, selenium, and ceria (Pt, Se, and CeO2, respectively). While it is understood that these nanoparticles have potential medical applications, there is a significant need to better understand both their potential therapeutic uses as well as any adverse toxic effects they may have. Thus it is necessary to further examine these nanoparticles and understand the full impact they have on health, particularly at the cellular and subcellular level. Furthermore, the effectiveness of these nanoparticles in the treatment of diseases, such as cancer and metabolic disorders including fibrotic diseases, needs to be better understood to fully exploit their utility in Nanomedicine. In this study, we evaluated the effects of three nanoparticles-Selenium (Se), Platinum (Pt) and Cerium (Ce) on primary mouse embryonic fibroblast cells. NPs were synthesized in the lab. Se NPs were produced via a chemical reduction of selenium ions using ascorbic acid as a reducing agent. PVP-coated Pt NPs were prepared by dissolution of Pt salts into water which chemically induced to convert to platinum atoms by using a reducing agent such as sodium borohydride NaBH4 using the method described by Park et al.(2002); PVP-coated cerium oxide nanoparticles NPs were synthesized as described previously by Merrifield et al. (2013). The physicochemical properties of SE, Pt and Ce NPs, such as morphology, size distribution, and surface potential, were determined. Cultured primary mouse embryonic fibroblast cells (MEFs) were exposed to Se (1, 25 and 50 μg/ml), Pt (1, 25, 50 μg/ml) and cerium (1, 25 and 50 μg/ml) nanoparticles for up to 6 days and evaluated for cell viability, proliferation, necrosis, DNA damage, and TGFB-1 signaling proteins expression by Immunoblotting. Results indicated: (1) Se NP induced the intrinsic pathway of apoptosis in primary mouse MEFs, at a minimal concentration of 1 μg Se/ml, without causing necrosis to the primary cells and may provide a new therapy for some metabolic and neoplastic diseases; (2) Pt NPs did not induce any toxicity in cell viability or lead to necrosis in MEFs, but significantly reduce proliferation by > ~ 50% and induction of TGFb-1 canonical pathway, causing production of endogenous collagen and a-smooth muscle actin (a-SMA) thus indicating it might serve a big role in the TGFB-1 signaling pathway in early stage cancer therapy but it may pose a hazard to patients with fibrotic diseases such as cardiac fibrosis; and (3) Cerium oxide nanoparticles (Nanoceria) were able to inhibit… Advisors/Committee Members: Geoffrey Scott.

Subjects/Keywords: Cancer; Fibrosis; Nanoceria; Platinum; Selenium; TGFB

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APA (6^th Edition):

Almurshidi, B. (2020). Selenium, Platinum and Cerium Oxide Nanoparticles' Applications to Cancer and Fibrotic Diseases in Medicine. (Doctoral Dissertation). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/5686

Chicago Manual of Style (16^th Edition):

Almurshidi, Badria. “Selenium, Platinum and Cerium Oxide Nanoparticles' Applications to Cancer and Fibrotic Diseases in Medicine.” 2020. Doctoral Dissertation, University of South Carolina. Accessed January 20, 2021. https://scholarcommons.sc.edu/etd/5686.

MLA Handbook (7^th Edition):

Almurshidi, Badria. “Selenium, Platinum and Cerium Oxide Nanoparticles' Applications to Cancer and Fibrotic Diseases in Medicine.” 2020. Web. 20 Jan 2021.

Vancouver:

Almurshidi B. Selenium, Platinum and Cerium Oxide Nanoparticles' Applications to Cancer and Fibrotic Diseases in Medicine. [Internet] [Doctoral dissertation]. University of South Carolina; 2020. [cited 2021 Jan 20]. Available from: https://scholarcommons.sc.edu/etd/5686.

Council of Science Editors:

Almurshidi B. Selenium, Platinum and Cerium Oxide Nanoparticles' Applications to Cancer and Fibrotic Diseases in Medicine. [Doctoral Dissertation]. University of South Carolina; 2020. Available from: https://scholarcommons.sc.edu/etd/5686

5. Lamers, Marcelo Lazzaron. Concentração elevada de glicose e interação célula-matriz extracelular: efeitos sobre a homeostase de glândulas salivares, adesão e migração celular.

Degree: PhD, Biologia Celular e Tecidual, 2008, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/42/42134/tde-11112008-131435/ ;

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Neste estudo avaliou-se os efeitos do diabetes mellitus (DM) sobre dois sistemas: glândula parótida de ratos e células cultivadas in vitro. Foram avaliados respectivamente a… (more)

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Neste estudo avaliou-se os efeitos do diabetes mellitus (DM) sobre dois sistemas: glândula parótida de ratos e células cultivadas in vitro. Foram avaliados respectivamente a composição da matriz extracelular e a migração de células expostas a elevada concentração de glicose. Na parótida observou-se aumento de colágenos III, IV e V, laminina e fibronectina, mediado por TGFb2. Em células isoladas observou-se que a glicose dificultou a polarização celular, reduziu a velocidade e direcionalidade de migração, reduziu a persistência e estabilidade das protrusões celulares e a maturação de adesões. Estas alterações estão relacionadas à ativação da GTPase Rac1, dependente de estresse oxidativo. Este estudo sugere, pela primeira vez, que: 1) a hipofunção salivar pode envolver um espessamento da lâmina basal de capilares e parênquima por mecanismos previamente observados em outros orgãos-alvo de complicações diabéticas e 2) que a glicose exerce um efeito direto sobre a migração celular, fator que pode contribuir para a cicatrização deficiente em indivíduos diabéticos.

In this study we evaluated the effects of DM on two different systems: the rat parotid gland and in vitro cultured cells. Extracellular matrix composition and the migratory behavior of cells exposed to a high glucose concentration (HG) were evaluated, respectively. In the parotid, DM led to an increase in collagens III, IV and V, laminin and fibronectin, through a TGFb2-dependent mechanism. In cultured cells, HG impaired cell polarization, reduced migration velocity and directionality, reduced the persistence and stability of protrusive cellular processes, as well as adhesion maturation. These effects were related to Rac1 GTPase activation, dependent on the oxidative stress promoted by HG. This study suggests, for the first time, that: 1) salivary hypofunction in DM might involve the thickening of capillary and parenchyma basal lamina, through mechanisms already described in other target organs for diabetic complications and 2) that glucose directly impairs cell migration, and this effect may contribute to the chronic wound healing observed in diabetic patients.

Advisors/Committee Members: Santos, Marinilce Fagundes dos.

Subjects/Keywords: Cell migration; Diabetes; Diabetes; Estresse oxidativo; Extracellular matrix; Glândula salivar; Matriz extracelular; Migração celular; Oxidative stress; Salivary gland; TGFb; TGFb

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APA (6^th Edition):

Lamers, M. L. (2008). Concentração elevada de glicose e interação célula-matriz extracelular: efeitos sobre a homeostase de glândulas salivares, adesão e migração celular. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42134/tde-11112008-131435/ ;

Chicago Manual of Style (16^th Edition):

Lamers, Marcelo Lazzaron. “Concentração elevada de glicose e interação célula-matriz extracelular: efeitos sobre a homeostase de glândulas salivares, adesão e migração celular.” 2008. Doctoral Dissertation, University of São Paulo. Accessed January 20, 2021. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-11112008-131435/ ;.

MLA Handbook (7^th Edition):

Lamers, Marcelo Lazzaron. “Concentração elevada de glicose e interação célula-matriz extracelular: efeitos sobre a homeostase de glândulas salivares, adesão e migração celular.” 2008. Web. 20 Jan 2021.

Vancouver:

Lamers ML. Concentração elevada de glicose e interação célula-matriz extracelular: efeitos sobre a homeostase de glândulas salivares, adesão e migração celular. [Internet] [Doctoral dissertation]. University of São Paulo; 2008. [cited 2021 Jan 20]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42134/tde-11112008-131435/ ;.

Council of Science Editors:

Lamers ML. Concentração elevada de glicose e interação célula-matriz extracelular: efeitos sobre a homeostase de glândulas salivares, adesão e migração celular. [Doctoral Dissertation]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/42/42134/tde-11112008-131435/ ;

Texas A&M University

6. Burns, Gregory Willis. Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15.

Degree: MS, Biomedical Sciences, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151804

► After 40 years of research, in vitro systems for mammalian embryo production produce lower quality embryos than those derived from in vivo sources. Recent reports… (more)

▼ After 40 years of research, in vitro systems for mammalian embryo production produce lower quality embryos than those derived from in vivo sources. Recent reports have demonstrated that in vitro bovine oocyte maturation systems benefit from the addition of oocyte secreted factors, specifically Bone Morphogenic Protein 15 (BMP15) from heterologous sources. However, known amino acid sequence variation and species-specific patterns of post-translational glycosylation lead us to hypothesize that utilization of bovine-specific oocyte secreted factors would be more beneficial than the observed effects of heterologous factors. To test this hypothesis, wild type, bovine BMP15 was cloned using reverse transcriptase PCR from RNA obtained from bovine ovarian tissue. For improved detection and purification of the biologically active recombinant protein, a FLAG tag peptide sequence (Asp-Tyr-Lys-Asp-Asp-Asp-Asp-Lys) was incorporated into the wild type BMP15 gene by PCR. This modified protein was cloned into the pCDNA 3 mammalian expression vector. HEK-293 (human embryonic kidney 293) and FBK (fetal bovine kidney) cell lines were transfected via electroporation and then selected to homogeneity. Collection and purification of rbFL-BMP15 from conditioned medium was accomplished by incubation with anti-FLAG affinity gel and the use of 3X FLAG peptide for elution. Peptides of 15.4 kDa and 17 kDa were noted from the human HEK-293 transfected cell line, while in contrast, bovine FBK cells produced a single 17 kDa protein. Bioactivity and BMP receptor signaling specificity were ascertained using in vitro treatment of HeLa cells and Western blotting for the BMP signaling molecule phosphorylated-SMAD 1/5. Inhibition of this signaling cascade using dorsomorphin, a selective bone morphogenic protein receptor I inhibitor, demonstrated the purified proteins served as BMP15-like agonists. To examine the impact of our purified, bovine-specific peptides on oocyte maturation, cumulus oocyte complexes were in vitro matured for 24 hours in the presence of 100 ng/ml recombinant human BMP15 or rbFL-BMP15 from human or bovine cell lines. Real time quantitative PCR analysis of BMP15 stimulated genes, PTGS2 and TSG6, revealed statistically significant increases in transcript level for treatment with human BMP15 by a Dunnett’s test (p<0.05). In this report, however, we failed to detect a significant affect of rbFL-BMP15 on the gene expression of in vitro mature cumulus oocyte complexes at 24 hours with 100 ng/ml rbFL-BMP15. Future studies including differing time points and concentrations, along with the addition of GDF9 to form a possible heterodimer should be investigated for the possibility of improving bovine oocyte in vitro maturation. Advisors/Committee Members: Long, Charles R (advisor), Golding, Michael C (committee member), Li, Qinglei (committee member).

Subjects/Keywords: BMP15; IVM; TGFB; recombinant protein; FLAG; BMPRI; ART; cattle; bovine; COC; oocyte

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APA (6^th Edition):

Burns, G. W. (2013). Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151804

Chicago Manual of Style (16^th Edition):

Burns, Gregory Willis. “Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15.” 2013. Masters Thesis, Texas A&M University. Accessed January 20, 2021. http://hdl.handle.net/1969.1/151804.

MLA Handbook (7^th Edition):

Burns, Gregory Willis. “Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15.” 2013. Web. 20 Jan 2021.

Vancouver:

Burns GW. Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15. [Internet] [Masters thesis]. Texas A&M University; 2013. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1969.1/151804.

Council of Science Editors:

Burns GW. Production and Functional Analysis of Recombinant Bovine Morphogenic Protein 15. [Masters Thesis]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151804

University of Guelph

7. Gilbert, Richard W.D. Characterization of TGFb signaling during epimorphic tissue regeneration: an example using the leopard gecko (Eublepharis macularius) tail regeneration model.

Degree: MS, Department of Biomedical Sciences, 2013, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/6609

► The transforming growth factor beta (TGFβ)/activin signaling pathway has a number of documented roles during wound healing and is becoming increasingly appreciated as a vital… (more)

Subjects/Keywords: TGFb; Activin; Smad; Regeneration; Scar Free Wound Healing; Leopard Gecko; Eublepharis macularius; EMT; Snail

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APA (6^th Edition):

Gilbert, R. W. D. (2013). Characterization of TGFb signaling during epimorphic tissue regeneration: an example using the leopard gecko (Eublepharis macularius) tail regeneration model. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/6609

Chicago Manual of Style (16^th Edition):

Gilbert, Richard W D. “Characterization of TGFb signaling during epimorphic tissue regeneration: an example using the leopard gecko (Eublepharis macularius) tail regeneration model.” 2013. Masters Thesis, University of Guelph. Accessed January 20, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/6609.

MLA Handbook (7^th Edition):

Gilbert, Richard W D. “Characterization of TGFb signaling during epimorphic tissue regeneration: an example using the leopard gecko (Eublepharis macularius) tail regeneration model.” 2013. Web. 20 Jan 2021.

Vancouver:

Gilbert RWD. Characterization of TGFb signaling during epimorphic tissue regeneration: an example using the leopard gecko (Eublepharis macularius) tail regeneration model. [Internet] [Masters thesis]. University of Guelph; 2013. [cited 2021 Jan 20]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/6609.

Council of Science Editors:

Gilbert RWD. Characterization of TGFb signaling during epimorphic tissue regeneration: an example using the leopard gecko (Eublepharis macularius) tail regeneration model. [Masters Thesis]. University of Guelph; 2013. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/6609

University of Adelaide

8. O'Leary, Sean. Seminal plasma cytokines as determinants of ovulation, embryo development and pregnancy success in the pig.

Degree: 2010, University of Adelaide

URL: http://hdl.handle.net/2440/63713

► Determinants of litter size in the pig are ovulation rate, fertilisation rate and embryo and fetal mortality. In practice, litter size is normally about half… (more)

▼ Determinants of litter size in the pig are ovulation rate, fertilisation rate and embryo and fetal mortality. In practice, litter size is normally about half the ovulation rate with 40% or more of potential piglets being lost before day 30 of pregnancy. Successful embryo development depends on optimal timing of events beginning with ovulation, fertilisation and preparation of the uterine environment for the attachment of the developing embryo. In the pig these processes are tightly controlled and are highly sensitive to disruption. The determinants of optimal early embryo development remain to be fully elucidated but evidence provided in mouse and human studies indicate that constituents of seminal plasma may provide a beneficial ‘priming’ stimulus acting at natural mating to synchronise and enhance early reproductive events. The cytokine transforming growth factor beta (TGFβ) is present in large quantities in mouse and human seminal plasma and is a principal active constituent in mediating seminal fluid signalling in the female reproductive tract. Experiments described in this thesis were designed to investigate whether boar seminal plasma can exert changes in the female reproductive tract during the pre-attachment period in the pig that are comparable to those described in mouse and human. Studies in this thesis demonstrate that seminal plasma causes a transient inflammatory response in the uterus characterised by induction of cytokine gene expression and immune cell changes that occur during the critical period in which the pig embryo is most vulnerable to demise. Seminal factors were also observed to enhance ovarian function, promoting synthesis of progesterone and influenced the rate of embryo development. The effect of these early changes due to seminal plasma was investigated in a large-scale field trial. However, this failed to demonstrate an effect of frozen-thawed seminal plasma on reproductive outcome in gilts. Moreover, the presumed active constituent of seminal plasma, TGFβ, was identified at high levels in boar semen but did not correlate with boar fertility. The information from these experiments provide a comprehensive understanding of mechanisms underlying the potentially beneficial actions of seminal plasma in early pregnancy. Ongoing studies will assist in the strategic design of (1) novel ‘surrogate seminal plasma’ or ‘semen extender’ products incorporating active constituents of seminal plasma, and (2) assays for measuring cytokine / immunoactive constituents of seminal plasma that are predictive of boar fertility. Advisors/Committee Members: Robertson, Sarah Anne (advisor), Armstrong, David Thomas (advisor), School of Paediatrics and Reproductive Health (school).

Subjects/Keywords: seminal plasma; pig; TGFB; cytokines; embryo development; determinants of ovulation; pregnancy; embryo survival

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APA (6^th Edition):

O'Leary, S. (2010). Seminal plasma cytokines as determinants of ovulation, embryo development and pregnancy success in the pig. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/63713

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

O'Leary, Sean. “Seminal plasma cytokines as determinants of ovulation, embryo development and pregnancy success in the pig.” 2010. Thesis, University of Adelaide. Accessed January 20, 2021. http://hdl.handle.net/2440/63713.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

O'Leary, Sean. “Seminal plasma cytokines as determinants of ovulation, embryo development and pregnancy success in the pig.” 2010. Web. 20 Jan 2021.

Vancouver:

O'Leary S. Seminal plasma cytokines as determinants of ovulation, embryo development and pregnancy success in the pig. [Internet] [Thesis]. University of Adelaide; 2010. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/2440/63713.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

O'Leary S. Seminal plasma cytokines as determinants of ovulation, embryo development and pregnancy success in the pig. [Thesis]. University of Adelaide; 2010. Available from: http://hdl.handle.net/2440/63713

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

9. SHWETA PRADIP JADHAV. STUDIES ON THE REGULATORY ROLES OF MICRORNA-27A AND MICRORNA-200B IN ACTIVATED RODENT MICROGLIA.

Degree: 2015, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/119890

Subjects/Keywords: miRNAs; microglia; inflammation; CNS; MAPK; TGFB

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APA (6^th Edition):

JADHAV, S. P. (2015). STUDIES ON THE REGULATORY ROLES OF MICRORNA-27A AND MICRORNA-200B IN ACTIVATED RODENT MICROGLIA. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/119890

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

JADHAV, SHWETA PRADIP. “STUDIES ON THE REGULATORY ROLES OF MICRORNA-27A AND MICRORNA-200B IN ACTIVATED RODENT MICROGLIA.” 2015. Thesis, National University of Singapore. Accessed January 20, 2021. http://scholarbank.nus.edu.sg/handle/10635/119890.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

JADHAV, SHWETA PRADIP. “STUDIES ON THE REGULATORY ROLES OF MICRORNA-27A AND MICRORNA-200B IN ACTIVATED RODENT MICROGLIA.” 2015. Web. 20 Jan 2021.

Vancouver:

JADHAV SP. STUDIES ON THE REGULATORY ROLES OF MICRORNA-27A AND MICRORNA-200B IN ACTIVATED RODENT MICROGLIA. [Internet] [Thesis]. National University of Singapore; 2015. [cited 2021 Jan 20]. Available from: http://scholarbank.nus.edu.sg/handle/10635/119890.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

JADHAV SP. STUDIES ON THE REGULATORY ROLES OF MICRORNA-27A AND MICRORNA-200B IN ACTIVATED RODENT MICROGLIA. [Thesis]. National University of Singapore; 2015. Available from: http://scholarbank.nus.edu.sg/handle/10635/119890

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

10. Padwal, Manreet. The Role of MMP9 and WNT Signaling in Peritoneal Angiogenesis.

Degree: PhD, 2017, McMaster University

URL: http://hdl.handle.net/11375/22089

► Patients on peritoneal dialysis (PD) are reliant on the peritoneum to provide a semi-permeable barrier to allow for dialysis (solute clearance), salt and water removal… (more)

▼ Patients on peritoneal dialysis (PD) are reliant on the peritoneum to provide a semi-permeable barrier to allow for dialysis (solute clearance), salt and water removal (ultrafiltration). PD patients are at risk of developing peritoneal fibrosis and angiogenesis which can lead to a decline in peritoneal membrane function. Specifically, PD patients develop increased solute transport and decreased osmotic conductance leading to ultrafiltration failure. Peritoneal angiogenesis is the leading factor that results in augmented peritoneal membrane solute transport which is associated with worse outcomes – increased risk of mortality and PD technique failure. Transforming growth factor beta (TGFB) is one of the primary cytokines involved in inducing epithelial to mesenchymal transition (EMT) and fibrosis. We hypothesize that PD leads to injury of the epithelial lining of the peritoneum – the mesothelial cells. These cells undergo a transition process and transitioned mesothelium are a source for angiogenic and fibrogenic growth factors. Matrix Metalloproteinase (MMP) 9 is an angiogeneic factor and has been observed to correlate with increased expression of vascular endothelial growth factor (VEGF). MMP9 has the ability to cleave and activate membrane bound factors such as E-cadherin and b-catenin respectively. There is substantial evidence that the canonical WNT/b-catenin pathway is active during fibrosis, and angiogenesis in different biological contexts. Thus, we investigated the role of MMP9 and WNT signaling in peritoneal angiogenesis. Limited evidence exists describing the role of noncanonical WNT signaling but some reports suggest that non-canonical WNT signaling inhibits WNT/b-catenin signaling. Non-canonical WNT5A has differential effects based on receptor context and has been shown to block WNT/b-catenin signaling in the presence of Receptor Tyrosine Kinase Like Orphan Receptor 2 (Ror2). The overall hypothesis of this PhD thesis is that MMP9 and WNT signaling play a key role in inducing peritoneal angiogenesis and are associated with changes in peritoneal membrane function. We expect WNT5A and Ror2 to protect against peritoneal membrane injury. From the overnight effluent of stable PD patients, we cultured mesothelial cells and assayed these for expression of MMP and WNT related genes. MMP9 and WNT1 gene expression were observed to be strongly correlated with peritoneal membrane solute transport in patients on PD. WNT2 mRNA was also positively correlated with peritoneal solute transport. We overexpressed MMP9 in the mouse peritoneum to demonstrate its role in angiogenesis and confirmed these findings using MMP9 -/- mice. In addition to this, we have shown a novel mechanism by which MMP9 induces angiogenesis by E-cadherin cleavage and b-catenin mediated signaling. The observed cross-talk between MMP9 and b-catenin prompted investigation of the activation of canonical WNT/b-catenin signaling in development of peritoneal membrane injury. In an experimental model of TGFB induced pertioneal injury, we confirmed the… Advisors/Committee Members: Margetts, Peter, Medical Sciences.

Subjects/Keywords: Peritoneal Dialysis; Angiogenesis; Fibrosis; Matrix Metalloproteinase 9; WNT/b-catenin signaling; TGFB; Epithelial to Mesenchymal Transition; WNT5A; Ror2; VEGF; Ultrafiltration

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Padwal, M. (2017). The Role of MMP9 and WNT Signaling in Peritoneal Angiogenesis. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/22089

Chicago Manual of Style (16^th Edition):

Padwal, Manreet. “The Role of MMP9 and WNT Signaling in Peritoneal Angiogenesis.” 2017. Doctoral Dissertation, McMaster University. Accessed January 20, 2021. http://hdl.handle.net/11375/22089.

MLA Handbook (7^th Edition):

Padwal, Manreet. “The Role of MMP9 and WNT Signaling in Peritoneal Angiogenesis.” 2017. Web. 20 Jan 2021.

Vancouver:

Padwal M. The Role of MMP9 and WNT Signaling in Peritoneal Angiogenesis. [Internet] [Doctoral dissertation]. McMaster University; 2017. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/11375/22089.

Council of Science Editors:

Padwal M. The Role of MMP9 and WNT Signaling in Peritoneal Angiogenesis. [Doctoral Dissertation]. McMaster University; 2017. Available from: http://hdl.handle.net/11375/22089

Université de Bordeaux I

11. Rottiers, Patricia. Etude de la formation des podosomes endothéliaux en réponse au TGFß : rôle essentiel du récepteur de type I, ALK1, et de la fibronectine dans un contexte d’activation de la cellule endothéliale : Study of endothelial podosomes formation induced by TGFβ : central role of type I receptor, ALK1; and of fibronectin in an active background of endothelial cell.

Degree: Docteur es, Biologie cellulaire et physiopathologie, 2009, Université de Bordeaux I

URL: http://www.theses.fr/2009BOR13983

►

Le TGFB(bêta) est un facteur clé dans l'homéostasie du réseau vasculaire. Le laboratoire a découvert que le TGFB(bêta) induit des podosomes dans les cellules endothéliales… (more)

▼

Le TGFB(bêta) est un facteur clé dans l'homéostasie du réseau vasculaire. Le laboratoire a découvert que le TGFB(bêta) induit des podosomes dans les cellules endothéliales (CE) artérielles in vitro. Ces microdomaines riches en F-actine, sont capables de dégrader localement la matrice extracellulaire. Nous avons mis en évidence des structures de même type dans l’endothélium natif, démontrant la pertinence des observations in vitro. Les CE expriment 2 récepteurs de type I au TGFB(bêta), ALK5 et ALK1, dont les fonctions respectives sur les CE font l’objet de controverses. Nous montrons in vitro, que l’assemblage des podosomes est dépendant de ALK1 et est induit dans un contexte d'activation de la CE. La fibronectine, présente dans la matrice lors de situations d'activation de la CE, est régulée par TGFB(bêta) /ALK1 dans notre modèle et est essentielle à la formation des podosomes. L'ensemble des données obtenues laisse présager un rôle des podosomes endothéliaux dans le remodelage artériel en réponse au TGFB(bêta).

TGFB(beta), a pleiotrop cytokine, acts as an important regulator for the maintenance of vascular homeostasis. Our team has discovered, for the first time, that TGFB(beta) induces podosomes formation in aortic endothelial cells (EC) in vitro. Podosomes are highly dynamic adhesion microdomains formed at the ventral membrane, consisting of a core of F-actin and actin-associated proteins, surrounded by a ring structure which in turn is consisting of plaque proteins as well as signaling proteins. In addition to the presence of specific markers, they are distinguished from other adhesion structures by the presence of metalloproteases, endowing them with the ability to degrade the extracellular matrix locally. We have bringing to light these structures in the endothelium of native arterial vessel exposed to biologically active TGFB(beta), showing relevance of these structures. Endothelial cells express two types I receptors of TGFB(beta), ALK5 and ALK1, which relative function on EC are controversial. We show in our model in vitro, that podosomes formation is ALK1-dependent and are induced when EC are in an active background. Fibronectin, an extracellular matrix component which is present during active situation, is regulated by TGFB(beta)/ALK1 signaling pathway and is essential for podosomes formation. This work open up new avenues to study the role of podosomes in vascular pathophysiology. We propose that podosomes are involved in arterial vessel remodeling.

Advisors/Committee Members: Génot, Elisabeth (thesis director).

Subjects/Keywords: Cellules endothéliales; TGFB(bêta); Podosomes; Fibronectine; ALK1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rottiers, P. (2009). Etude de la formation des podosomes endothéliaux en réponse au TGFß : rôle essentiel du récepteur de type I, ALK1, et de la fibronectine dans un contexte d’activation de la cellule endothéliale : Study of endothelial podosomes formation induced by TGFβ : central role of type I receptor, ALK1; and of fibronectin in an active background of endothelial cell. (Doctoral Dissertation). Université de Bordeaux I. Retrieved from http://www.theses.fr/2009BOR13983

Chicago Manual of Style (16^th Edition):

Rottiers, Patricia. “Etude de la formation des podosomes endothéliaux en réponse au TGFß : rôle essentiel du récepteur de type I, ALK1, et de la fibronectine dans un contexte d’activation de la cellule endothéliale : Study of endothelial podosomes formation induced by TGFβ : central role of type I receptor, ALK1; and of fibronectin in an active background of endothelial cell.” 2009. Doctoral Dissertation, Université de Bordeaux I. Accessed January 20, 2021. http://www.theses.fr/2009BOR13983.

MLA Handbook (7^th Edition):

Rottiers, Patricia. “Etude de la formation des podosomes endothéliaux en réponse au TGFß : rôle essentiel du récepteur de type I, ALK1, et de la fibronectine dans un contexte d’activation de la cellule endothéliale : Study of endothelial podosomes formation induced by TGFβ : central role of type I receptor, ALK1; and of fibronectin in an active background of endothelial cell.” 2009. Web. 20 Jan 2021.

Vancouver:

Rottiers P. Etude de la formation des podosomes endothéliaux en réponse au TGFß : rôle essentiel du récepteur de type I, ALK1, et de la fibronectine dans un contexte d’activation de la cellule endothéliale : Study of endothelial podosomes formation induced by TGFβ : central role of type I receptor, ALK1; and of fibronectin in an active background of endothelial cell. [Internet] [Doctoral dissertation]. Université de Bordeaux I; 2009. [cited 2021 Jan 20]. Available from: http://www.theses.fr/2009BOR13983.

Council of Science Editors:

Rottiers P. Etude de la formation des podosomes endothéliaux en réponse au TGFß : rôle essentiel du récepteur de type I, ALK1, et de la fibronectine dans un contexte d’activation de la cellule endothéliale : Study of endothelial podosomes formation induced by TGFβ : central role of type I receptor, ALK1; and of fibronectin in an active background of endothelial cell. [Doctoral Dissertation]. Université de Bordeaux I; 2009. Available from: http://www.theses.fr/2009BOR13983

NSYSU

12. Hsu, Ya-Wen. Epithelial membrane protein 2 inhibits cell proliferation and induces apoptosis via TGFB-SP1 axis and recruitment of P2RX7 in urinary bladder urothelial carcinoma-derived cells.

Degree: Master, Institute of Biomedical Sciences, 2018, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0611118-123519

► In this study, our objective was to investigate the mechanisms of Epithelial membrane protein 2 (EMP2) inhibits cell proliferation and induces apoptosis in urinary bladder… (more)

Subjects/Keywords: SP1 (Specificity protein-1); TGFB; Epithelial membrane protein 2 (EMP2); Urinary bladder urothelial carcinoma (UBUC); Cell cycle arrest

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APA (6^th Edition):

Hsu, Y. (2018). Epithelial membrane protein 2 inhibits cell proliferation and induces apoptosis via TGFB-SP1 axis and recruitment of P2RX7 in urinary bladder urothelial carcinoma-derived cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0611118-123519

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hsu, Ya-Wen. “Epithelial membrane protein 2 inhibits cell proliferation and induces apoptosis via TGFB-SP1 axis and recruitment of P2RX7 in urinary bladder urothelial carcinoma-derived cells.” 2018. Thesis, NSYSU. Accessed January 20, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0611118-123519.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hsu, Ya-Wen. “Epithelial membrane protein 2 inhibits cell proliferation and induces apoptosis via TGFB-SP1 axis and recruitment of P2RX7 in urinary bladder urothelial carcinoma-derived cells.” 2018. Web. 20 Jan 2021.

Vancouver:

Hsu Y. Epithelial membrane protein 2 inhibits cell proliferation and induces apoptosis via TGFB-SP1 axis and recruitment of P2RX7 in urinary bladder urothelial carcinoma-derived cells. [Internet] [Thesis]. NSYSU; 2018. [cited 2021 Jan 20]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0611118-123519.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hsu Y. Epithelial membrane protein 2 inhibits cell proliferation and induces apoptosis via TGFB-SP1 axis and recruitment of P2RX7 in urinary bladder urothelial carcinoma-derived cells. [Thesis]. NSYSU; 2018. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0611118-123519

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

13. Martin, Marion. Analyse de la méthylation de l'ADN des cellules CD133+ dans le cancer du foie et son interaction avec la voie de signalisation TGF-b : Identification of a DNA methylation signature in CD133+ liver cancer cell lines and its relation with the transforming growth factor beta signaling pathway.

Degree: Docteur es, Sciences de la Vie, 2013, Lyon, École normale supérieure

URL: http://www.theses.fr/2013ENSL0862

► Au sein des tumeurs, y compris pour le carcinome hépatocellulaire (CHC), des sous-populations de cellules néoplasiques ont révélé une grande capacité à initier de nouvelles… (more)

▼ Au sein des tumeurs, y compris pour le carcinome hépatocellulaire (CHC), des sous-populations de cellules néoplasiques ont révélé une grande capacité à initier de nouvelles tumeurs et à induire des métastases. Les premières études sur ces cellules ont rapidement montré que la présence de ces cellules était déterminante dans le développement tumoral et elles ont donc été renommées « cellules souches cancéreuses » (CSCs). Malheureusement les mécanismes impliqués dans la maintenance de ces CSCs ne sont que partiellement compris. Par ailleurs dans le CHC un lien a été établi entre les signaux du facteur de croissance de transformation (Transforming Growth Factor, TGF-ß) provenant du microenvironnement tumoral et certaines populations de cellules cancéreuses dont la présence est corrélée à un faible pronostic. La façon dont TGF-ß peut ainsi établir et modifier un phénotype cellulaire dans le CHC reste néanmoins obscure. La méthylation de l’ADN étant un acteur majeur dans la mise en place des programmes cellulaires, notre but a été de caractériser le méthylome de CSCs hépatiques et son lien avec la capacité de TGF-ß à induire des CSCs. Nous nous sommes appuyés sur l’expression du marqueur CD133 pour définir la population de CSCs hépatiques. Afin comprendre l’importance des marques de méthylation de l’ADN dans les CSCs hépatiques, nous avons dans un premier temps déterminé quelle était la signature des cellules CD133+ au niveau de la méthylation de l’ADN en utilisant des puces de méthylation à grande échelle. Les sites CpG différentiellement méthylés ont montré un enrichissement pour d’une part des voies de signalisation déjà identifiées dans les CSCs et, d’autre part, pour des voies de signalisation associées au processus inflammatoire dont la voie TGF-ß/SMAD. Par la suite, nous avons montré que TGF-ß pouvait induire de façon permanente les cellules CD133+ contrairement à une autre cytokine influente dans le cancer du foie, l’interleukine 6. Cette augmentation de cellules CD133+ induite par TGF-ß est associée à des changements de méthylation de l’ADN sur l’ensemble du génome et qui sont, de plus, maintenus au cours des divisions cellulaires. La comparaison entre les deux méthylomes (liés aux cellules CD133+ et à l’action de TGF-ß) a exposé une signature commune significative indiquant que TGF-ß pourrait promouvoir le phénotype de CSC via le processus de méthylation de l’ADN. Mais nous avons également déterminé qu’une grande partie des effets sur la méthylation induits par TGF-ß était totalement indépendante de l’induction de cellules CD133+. Enfin, nous avons observé que les sites de méthylation sensibles au signal de TGF-ß étaient regroupés de façon significative au niveau de régions « enhancer » qui régulent la transcription des gènes. Par ailleurs, ces sites incluaient également des gènes précédemment identifiés comme cibles de TGF-ß mais aussi des gènes codant pour des acteurs épigénétiques de premier ordre comme les méthyltransférases de l’ADN. Ces résultats constituent la première description d’une signature de… Advisors/Committee Members: Herceg, Zdenko (thesis director).

Subjects/Keywords: Carcinome Hepatocelllulaire; Cellules souches cancéreuses; CD133; Méthylation de l'ADN; TGF-beta; Hepatocellular carcinoma; Cancer stem cells; CD133; DNA methylation; TGFb pathway

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Martin, M. (2013). Analyse de la méthylation de l'ADN des cellules CD133+ dans le cancer du foie et son interaction avec la voie de signalisation TGF-b : Identification of a DNA methylation signature in CD133+ liver cancer cell lines and its relation with the transforming growth factor beta signaling pathway. (Doctoral Dissertation). Lyon, École normale supérieure. Retrieved from http://www.theses.fr/2013ENSL0862

Chicago Manual of Style (16^th Edition):

Martin, Marion. “Analyse de la méthylation de l'ADN des cellules CD133+ dans le cancer du foie et son interaction avec la voie de signalisation TGF-b : Identification of a DNA methylation signature in CD133+ liver cancer cell lines and its relation with the transforming growth factor beta signaling pathway.” 2013. Doctoral Dissertation, Lyon, École normale supérieure. Accessed January 20, 2021. http://www.theses.fr/2013ENSL0862.

MLA Handbook (7^th Edition):

Martin, Marion. “Analyse de la méthylation de l'ADN des cellules CD133+ dans le cancer du foie et son interaction avec la voie de signalisation TGF-b : Identification of a DNA methylation signature in CD133+ liver cancer cell lines and its relation with the transforming growth factor beta signaling pathway.” 2013. Web. 20 Jan 2021.

Vancouver:

Martin M. Analyse de la méthylation de l'ADN des cellules CD133+ dans le cancer du foie et son interaction avec la voie de signalisation TGF-b : Identification of a DNA methylation signature in CD133+ liver cancer cell lines and its relation with the transforming growth factor beta signaling pathway. [Internet] [Doctoral dissertation]. Lyon, École normale supérieure; 2013. [cited 2021 Jan 20]. Available from: http://www.theses.fr/2013ENSL0862.

Council of Science Editors:

Martin M. Analyse de la méthylation de l'ADN des cellules CD133+ dans le cancer du foie et son interaction avec la voie de signalisation TGF-b : Identification of a DNA methylation signature in CD133+ liver cancer cell lines and its relation with the transforming growth factor beta signaling pathway. [Doctoral Dissertation]. Lyon, École normale supérieure; 2013. Available from: http://www.theses.fr/2013ENSL0862

14. Guerrero Zayas, Mara Isel. Designing New Approaches for the Study of Early Murine Endodermal Organogenesis using Whole Embryo Culture.

Degree: MS(M.S.), Animal Science, 2011, U of Massachusetts : Masters

URL: http://scholarworks.umass.edu/theses/561

► This thesis investigates the applicability of novel approaches designed to study the molecular mechanisms required for the initiation of organogenesis within the early endoderm. The… (more)

▼ This thesis investigates the applicability of novel approaches designed to study the molecular mechanisms required for the initiation of organogenesis within the early endoderm. The endoderm is the germ layer that gives rise to the gut-tube and associated organs including the thyroid, lung, liver and pancreas. Our laboratory focuses on understanding the molecular mechanisms governing the developmental transition from endoderm to liver and pancreas. Several signaling pathways including Wnt, Retinoic Acid (RA), Bone Morphogenetic Protein (BMP) and Transforming Growth Factor-β (TGFβ) have been implicated in the emergence of the liver bud from the endoderm in the mouse or other vertebrate species. However, neither the exact signals nor the precise roles during budding process have been identified, due to the complexity of specifically altering these essential pathways using traditional genetic approaches during the earliest stages of endoderm organogenesis. These traditional techniques include transgenic, knockout or conditional knockouts strategies. To overcome the difficulties of genetic accessibility, our laboratory has optimized two complementary approaches, electroporation and addition of activators or inhibitors directly to the culture media, to study the earliest stages of organ formation using an ex vivo culture system (whole embryo culture), that allow us for normal embryonic development for up to two days. This ex-vivo technique also provides the opportunity to access and manipulate the endoderm, specifically the liver and pancreas precursor cells, prior to organ specification. Because the endoderm undergoes normal liver and pancreas specification in our ex vivo system by 24 hours after culture begin, we reason that it is possible to manipulate gene expression at the onset of culture. We then determine the effects of this manipulation on liver or pancreas development by molecular and morphological analysis after culture. The first approach we developed is the use of directional electroporation of nucleic acids to manipulate a specific region of the endoderm, particularly on liver and pancreas developmental processes. The second method is global inhibition or activation using inhibitors or growth factors activators, focusing on the TGFβ signaling pathway. These techniques will be performed prior to, or concurrent with, liver and pancreas specification, followed by embryo culture until after the onset of organogenesis. The combination of these techniques constitutes a practical approach to stage-manage the endoderm in a temporally and spatially distinct manner. In addition, it will allow us to alter specific signaling pathways without the labor-intensive generation of genetically modified animals. Indeed, establishment of these methodologies may provide a robust tool for rapid screening of candidate genes and signaling molecules underlying organogenesis in any endodermally derived organ in mouse embryos. Advisors/Committee Members: Kimberly D. Tremblay.

Subjects/Keywords: Whole Embryo Culture; Electroporation; Endoderm Organogenesis; Small Molecules or Growth Factors; Liver and Pancreas Development; TGFB; Other Animal Sciences

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APA (6^th Edition):

Guerrero Zayas, M. I. (2011). Designing New Approaches for the Study of Early Murine Endodermal Organogenesis using Whole Embryo Culture. (Masters Thesis). U of Massachusetts : Masters. Retrieved from http://scholarworks.umass.edu/theses/561

Chicago Manual of Style (16^th Edition):

Guerrero Zayas, Mara Isel. “Designing New Approaches for the Study of Early Murine Endodermal Organogenesis using Whole Embryo Culture.” 2011. Masters Thesis, U of Massachusetts : Masters. Accessed January 20, 2021. http://scholarworks.umass.edu/theses/561.

MLA Handbook (7^th Edition):

Guerrero Zayas, Mara Isel. “Designing New Approaches for the Study of Early Murine Endodermal Organogenesis using Whole Embryo Culture.” 2011. Web. 20 Jan 2021.

Vancouver:

Guerrero Zayas MI. Designing New Approaches for the Study of Early Murine Endodermal Organogenesis using Whole Embryo Culture. [Internet] [Masters thesis]. U of Massachusetts : Masters; 2011. [cited 2021 Jan 20]. Available from: http://scholarworks.umass.edu/theses/561.

Council of Science Editors:

Guerrero Zayas MI. Designing New Approaches for the Study of Early Murine Endodermal Organogenesis using Whole Embryo Culture. [Masters Thesis]. U of Massachusetts : Masters; 2011. Available from: http://scholarworks.umass.edu/theses/561

University of Cambridge

15. Sedikides, George. Characterisation of T cell responses to proteins expressed during Human Cytomegalovirus latency.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/293985

► Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes a lifelong infection in hosts. In the majority of cases, the immune response to primary HCMV infection… (more)

▼ Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes a lifelong infection in hosts. In the majority of cases, the immune response to primary HCMV infection limits viral replication and dissemination, such that overt clinical disease is prevented. However, the immune system cannot prevent the virus establishing a latent infection, which enables lifelong persistence. Historically, a long-standing view was that viral gene expression during latency was largely absent, thus facilitating the avoidance of immune detection. However, it has now been established that viral activity in latency is far from quiescent, and the expression of a number of viral genes is known to occur. Therefore, an important question arises: are T cells specific to these proteins generated, and, if so, why are HCMV latently infected cells maintained in the face of these potential T cell responses? Previous work has shown that two such viral gene products, UL138 and LUNA, are recognised by CD4+ T cells, with a subpopulation of these cells secreting the immunosuppressive cytokines interleukin (IL)-10 and transforming growth factor beta (β). However, little is known about the host immune response to other key latency-associated viral proteins; US28, UL111A, and UL144. Using overlapping peptide pools designed to cover the whole of the predicted amino acid sequence of these HCMV proteins, in combination with fluorescent ELIspot (FluoroSpot), ELISA, and intracellular cytokine staining, I have determined the frequency, cytokine secretion profile, effector function, and memory phenotype of CD4+ and CD8+ T cells in a large cohort of HCMV seropositive healthy donors. My results show that these viral gene products are also recognised by CD4+ T cells and are composed of distinct cellular populations secreting either IFNγ or IL-10. The high sensitivity of this assay has also revealed previously uncharacterised CD8+ T cell responses to US28, UL111A, and UL144, as well as responses to LUNA and UL138. Intriguingly, IL-10 secretion by a distinct population of latency-specific CD8+ T cells was also observed. T cell responses to latency-associated ORF products were found to be composed of greater proportions of IL-10 secreting cells compared to responses to the lytic ORFs pp65, IE1, and gB. The frequencies of IL-10 secreting T cells specific to HCMV latency-associated proteins did not increase with greater time of viral carriage, as measured indirectly by donor age. Although IFNγ secreting T cells specific to latency-associated proteins were detected in kidney transplant recipients immediately following primary HCMV infection, there were no such IL-10 secreting sub-populations, despite IL-10 T cell responses being detected to two lytic proteins, US3 and pp71. Given that latency-specific IL-10 secreting T cells were found to be a separate population to those secreting IFNγ, it was hypothesised that depleting the IL-10 secreting cells could improve the recognition and killing of latently infected cells by the specific but…

Subjects/Keywords: hcmv; cmv; human cytomegalovirus; il-10; tgfb; viral latency; T cells; latency; Immune manipulation; immune evasion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sedikides, G. (2019). Characterisation of T cell responses to proteins expressed during Human Cytomegalovirus latency. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/293985

Chicago Manual of Style (16^th Edition):

Sedikides, George. “Characterisation of T cell responses to proteins expressed during Human Cytomegalovirus latency.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 20, 2021. https://www.repository.cam.ac.uk/handle/1810/293985.

MLA Handbook (7^th Edition):

Sedikides, George. “Characterisation of T cell responses to proteins expressed during Human Cytomegalovirus latency.” 2019. Web. 20 Jan 2021.

Vancouver:

Sedikides G. Characterisation of T cell responses to proteins expressed during Human Cytomegalovirus latency. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 20]. Available from: https://www.repository.cam.ac.uk/handle/1810/293985.

Council of Science Editors:

Sedikides G. Characterisation of T cell responses to proteins expressed during Human Cytomegalovirus latency. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/293985

16. SIM WEN JING. MECHANISMS GOVERNING EPITHELIAL MESENCHYMAL TRANSITION IN BLADDER CARCINOMA.

Degree: 2013, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/53379

Subjects/Keywords: epithelial mesenchymal transition; bladder cancer; TGFb; HGF; MAPK; invasion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

JING, S. W. (2013). MECHANISMS GOVERNING EPITHELIAL MESENCHYMAL TRANSITION IN BLADDER CARCINOMA. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/53379

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

JING, SIM WEN. “MECHANISMS GOVERNING EPITHELIAL MESENCHYMAL TRANSITION IN BLADDER CARCINOMA.” 2013. Thesis, National University of Singapore. Accessed January 20, 2021. http://scholarbank.nus.edu.sg/handle/10635/53379.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

JING, SIM WEN. “MECHANISMS GOVERNING EPITHELIAL MESENCHYMAL TRANSITION IN BLADDER CARCINOMA.” 2013. Web. 20 Jan 2021.

Vancouver:

JING SW. MECHANISMS GOVERNING EPITHELIAL MESENCHYMAL TRANSITION IN BLADDER CARCINOMA. [Internet] [Thesis]. National University of Singapore; 2013. [cited 2021 Jan 20]. Available from: http://scholarbank.nus.edu.sg/handle/10635/53379.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

JING SW. MECHANISMS GOVERNING EPITHELIAL MESENCHYMAL TRANSITION IN BLADDER CARCINOMA. [Thesis]. National University of Singapore; 2013. Available from: http://scholarbank.nus.edu.sg/handle/10635/53379

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

17. Sedikides, George. Characterisation of T cell responses to proteins expressed during human cytomegalovirus latency.

Degree: PhD, 2019, University of Cambridge

URL: https://doi.org/10.17863/CAM.41093 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782839

► Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes a lifelong infection in hosts. In the majority of cases, the immune response to primary HCMV infection… (more)

▼ Human cytomegalovirus (HCMV) is a betaherpesvirus that establishes a lifelong infection in hosts. In the majority of cases, the immune response to primary HCMV infection limits viral replication and dissemination, such that overt clinical disease is prevented. However, the immune system cannot prevent the virus establishing a latent infection, which enables lifelong persistence. Historically, a long-standing view was that viral gene expression during latency was largely absent, thus facilitating the avoidance of immune detection. However, it has now been established that viral activity in latency is far from quiescent, and the expression of a number of viral genes is known to occur. Therefore, an important question arises: are T cells specific to these proteins generated, and, if so, why are HCMV latently infected cells maintained in the face of these potential T cell responses? Previous work has shown that two such viral gene products, UL138 and LUNA, are recognised by CD4+ T cells, with a subpopulation of these cells secreting the immunosuppressive cytokines interleukin (IL)-10 and transforming growth factor beta (β). However, little is known about the host immune response to other key latency-associated viral proteins; US28, UL111A, and UL144. Using overlapping peptide pools designed to cover the whole of the predicted amino acid sequence of these HCMV proteins, in combination with fluorescent ELIspot (FluoroSpot), ELISA, and intracellular cytokine staining, I have determined the frequency, cytokine secretion profile, effector function, and memory phenotype of CD4+ and CD8+ T cells in a large cohort of HCMV seropositive healthy donors. My results show that these viral gene products are also recognised by CD4+ T cells and are composed of distinct cellular populations secreting either IFNγ or IL-10. The high sensitivity of this assay has also revealed previously uncharacterised CD8+ T cell responses to US28, UL111A, and UL144, as well as responses to LUNA and UL138. Intriguingly, IL-10 secretion by a distinct population of latency-specific CD8+ T cells was also observed. T cell responses to latency-associated ORF products were found to be composed of greater proportions of IL-10 secreting cells compared to responses to the lytic ORFs pp65, IE1, and gB. The frequencies of IL-10 secreting T cells specific to HCMV latency-associated proteins did not increase with greater time of viral carriage, as measured indirectly by donor age. Although IFNγ secreting T cells specific to latency-associated proteins were detected in kidney transplant recipients immediately following primary HCMV infection, there were no such IL-10 secreting sub-populations, despite IL-10 T cell responses being detected to two lytic proteins, US3 and pp71. Given that latency-specific IL-10 secreting T cells were found to be a separate population to those secreting IFNγ, it was hypothesised that depleting the IL-10 secreting cells could improve the recognition and killing of latently infected cells by the specific but non-IL-10 producing T cell…

Subjects/Keywords: hcmv; cmv; human cytomegalovirus; il-10; tgfb; viral latency; T cells; latency; Immune manipulation; immune evasion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sedikides, G. (2019). Characterisation of T cell responses to proteins expressed during human cytomegalovirus latency. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.41093 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782839

Chicago Manual of Style (16^th Edition):

Sedikides, George. “Characterisation of T cell responses to proteins expressed during human cytomegalovirus latency.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 20, 2021. https://doi.org/10.17863/CAM.41093 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782839.

MLA Handbook (7^th Edition):

Sedikides, George. “Characterisation of T cell responses to proteins expressed during human cytomegalovirus latency.” 2019. Web. 20 Jan 2021.

Vancouver:

Sedikides G. Characterisation of T cell responses to proteins expressed during human cytomegalovirus latency. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 20]. Available from: https://doi.org/10.17863/CAM.41093 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782839.

Council of Science Editors:

Sedikides G. Characterisation of T cell responses to proteins expressed during human cytomegalovirus latency. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.41093 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782839

University of Texas – Austin

18. -8457-8886. High throughput platforms for studying dynamic cellular mechanobiology.

Degree: PhD, Biomedical Engineering, 2016, University of Texas – Austin

URL: http://hdl.handle.net/2152/68255

► Cardiovascular disease is one of the most common causes of death in the US and the world. On average, $312 billion is spent every year… (more)

▼ Cardiovascular disease is one of the most common causes of death in the US and the world. On average, $312 billion is spent every year in drug development and treatment for more than 200 drugs in development by 2013. Despite the resources available, no therapy exists that can effectively treat vascular disease. The chronic nature of the disease renders various treatment methods ineffective on the long term. Drugs with promising preliminary results often fail to succeed in clinical trials. Those that do pass the clinical trial stages require an average of 12 years of development time before they are commercially available. Many of these treatments fail from the poor representation of the dynamic mechanical forces that direct tissue behavior in the body. Previous studies have shown that mechanobiology plays a significant role from a cellular level. These studies have revealed a variety of mechanisms through which mechanical forces can alter cardiovascular biology. Mechanical forces can interact with cellular structures through the transmission of force to other elements and through transduction to turn mechanical forces into a chemical event. The search for potential molecular mechanotransducers has revealed a variety of complex and fascinating mechanisms through which stretch- and flow-induced forces can alter arterial biology. Although these pathways are known to be involved in sensing forces, much remains to be understood as to how these pathways work together to guide its downstream effects or how to engineer efficient therapies for disease. The lack of tools to accurately capture these mechanical forces is a major barrier in anticipating treatment response in vivo. Thus, there is a large disconnect between in vitro and in vivo results. Consequently, there is a high demand to effectively mimic the mechanical environment of the body. Development of in vivo techniques that can produce the necessary strains and stresses can be the key in expediting the transition from preliminary research into clinical trials. Preemptively exposing the cells to the complex physiological forces at high throughput could screen out for multitude of small molecule treatments that can be ineffective in vivo before beginning clinical trials. The results could also reveal potential therapeutic targets that affect disease progression and also condition mesenchymal stem cells and vascular cells to the mechanical stresses to promote proper differentiation and remodeling. Here we have designed and developed a device that is capable of depicting the physiological forces at high throughput with high accuracy and flexibility. Throughout the course of this research we have demonstrated its capability to explore cellular response to ranges of dynamic mechanical strain. Using this advantage, we have examined the changes in vascular smooth muscle cells, and studied the potential to use mechanical strain to condition human mesenchymal stem cell to have endothelial phenotypes and endothelial cells to have mesenchymal phenotypes. Advisors/Committee Members: Baker, Aaron Blair (advisor), Kim, Jonghwan (committee member), Lu, Nanshu (committee member), Sacks, Michael S (committee member), Suggs, Laura J (committee member).

Subjects/Keywords: Mechanobiology; Mesenchymal stem cell; Vascular smooth muscle cell; Cyclic strain waveform; Tgfb; Endothelial mesenchymal transition; Endmt; Hippo

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

-8457-8886. (2016). High throughput platforms for studying dynamic cellular mechanobiology. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/68255

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Chicago Manual of Style (16^th Edition):

-8457-8886. “High throughput platforms for studying dynamic cellular mechanobiology.” 2016. Doctoral Dissertation, University of Texas – Austin. Accessed January 20, 2021. http://hdl.handle.net/2152/68255.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7^th Edition):

-8457-8886. “High throughput platforms for studying dynamic cellular mechanobiology.” 2016. Web. 20 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-8457-8886. High throughput platforms for studying dynamic cellular mechanobiology. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2016. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/2152/68255.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

-8457-8886. High throughput platforms for studying dynamic cellular mechanobiology. [Doctoral Dissertation]. University of Texas – Austin; 2016. Available from: http://hdl.handle.net/2152/68255

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

19. Ramachandran, Kalyani Nithya. PROTECTIVE ROLES OF miR-29a AND miR-18a IN LIVER FIBROSIS.

Degree: 2013, Johns Hopkins University

URL: http://jhir.library.jhu.edu/handle/1774.2/36948

► The research described in this dissertation highlights the need for clinical therapeutics for fibrosis, targeting fibrotic mechanisms and how miRNAs can be powerful modulators of… (more)

▼ The research described in this dissertation highlights the need for clinical therapeutics for fibrosis, targeting fibrotic mechanisms and how miRNAs can be powerful modulators of fibrosis. miRNAs are 22 nucleotide long, post-transcriptional regulators of gene expression. We profiled miRNA expression changes in two different models of liver fibrosis and identified two different miRNAs which showed differential expression in fibrotic livers. miR-29 family targets many proteins in the extracellular matrix and is downregulated during fibrosis in many organs. We developed a viral vector based delivery of miR-29 to replace lost miR-29 during fibrosis. Successful prevention and reversal of ongoing hepatotoxin mediated fibrosis was seen with hepatocyte-specific expression of the viral vector, illustrating the powerful anti-fibrotic role of miR-29. Our research supports and encourages industry interest in developing miR-29 based drugs, which takes us one step closer to alleviating distress of patients in the clinic. Alcohol mediated fibrosis is a major health problem in the world and is the major cause contributing to the increased need for liver transplantation. We studied miR-18a, which is increased in alcohol and hepatotoxin mediated liver fibrosis. miR-18a expression is localized to cells in the same region as fibroblasts, which are the key responders in fibrosis. This miRNA targets components of TGFB signaling pathway and affects pro-fibrotic processes such as fibroblast migration and collagen production. miR-18a is downregulated by TGFB, illustrating that TGFB downregulates its own negative regulator, fine-tuning signaling activity. Combined, these results strongly suggest a protective role of miR-18a during liver fibrosis. This work establishes a large body of knowledge about miRNAs and their roles in regulating fibrosis. We identified cell type specific expression and function of miRNAs within the liver that further confirms the need to look not only at whole tissue expression but also in different individual cells. We have highlighted the role of miRNAs in regulating and therapeutically treating liver fibrosis and hope that clinical drugs of miRNAs would not be too far in the future. Advisors/Committee Members: Valle, David (advisor).

Subjects/Keywords: Liver fibrosis; miRNA; miR-29a; miR-18a; TGFB pathway

11 more images…

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APA (6^th Edition):

Ramachandran, K. N. (2013). PROTECTIVE ROLES OF miR-29a AND miR-18a IN LIVER FIBROSIS. (Thesis). Johns Hopkins University. Retrieved from http://jhir.library.jhu.edu/handle/1774.2/36948

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ramachandran, Kalyani Nithya. “PROTECTIVE ROLES OF miR-29a AND miR-18a IN LIVER FIBROSIS.” 2013. Thesis, Johns Hopkins University. Accessed January 20, 2021. http://jhir.library.jhu.edu/handle/1774.2/36948.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ramachandran, Kalyani Nithya. “PROTECTIVE ROLES OF miR-29a AND miR-18a IN LIVER FIBROSIS.” 2013. Web. 20 Jan 2021.

Vancouver:

Ramachandran KN. PROTECTIVE ROLES OF miR-29a AND miR-18a IN LIVER FIBROSIS. [Internet] [Thesis]. Johns Hopkins University; 2013. [cited 2021 Jan 20]. Available from: http://jhir.library.jhu.edu/handle/1774.2/36948.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ramachandran KN. PROTECTIVE ROLES OF miR-29a AND miR-18a IN LIVER FIBROSIS. [Thesis]. Johns Hopkins University; 2013. Available from: http://jhir.library.jhu.edu/handle/1774.2/36948

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. Βουμβουράκη, Αργυρώ. Ο ρόλος της οκτρεοτίδης ως αντιϊνωτικού παράγοντα σε ασθενείς με χρόνια ηπατοπάθεια.

Degree: 2010, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/25020

►

Liver fibrosis is a dynamic phenomenon, the progression of which depends upon the activation of hepatic stellate cells. The production of extracellular matrix protein is… (more)

▼

Liver fibrosis is a dynamic phenomenon, the progression of which depends upon the activation of hepatic stellate cells. The production of extracellular matrix protein is regulated by many cytokines while clinical evaluation of patients with chronic liver disease demands a regular evaluation of the fibrotic process. Until now liver biopsy remains the gold standard, but it is an invasive procedure with some degree of morbidity. Moreover, therapeutic substances might negatively influence the development of fibrosis with detrimental results. Octreotide, a synthetic somatostatin, is widely used for the control of variceal bleeding and the therapy of HCC. The effect of Octreotide in the process of fibrosis has not been studied. AIM: To study the effect of Octreotide on serum parameters related to fibrosis of patients with chronic liver disease. ΜETHODS: Serum proteins that have been shown to be associated with the fibrotic process were chosen. Four groups of proteins were studied: a) Leptin, Laminin, Collagen-IV and Hyaluronan were measured in the peripheral blood of patients with chronic liver disease as well as in the hepatic vein blood after catheterization of cirrhotic patients. Areas Under the Curve (AUC) were created to investigate the possibility of discrimination between patients with chronic viral hepatitis and viral cirrhosis, as well as the possibility of discrimination between patients with early PBC and advanced PBC. The effect of Octreotide on serum levels of these factors was also studied. Measurements were done with commercially available ELISAs. b) In the same patients, the group of TGFb proteins (TGFb1, TGFb2, TGFb3) and the effect of Octreotide in their levels were also biochemically studied (ELISA). Moreover, in this part we used histochemistry (methods of alkaline phosphatase and immunofluorescence) to localize these proteins in the hepatic tissue. Also, in a limited number of hepatic tissues the mRNA expression of the protein FoxP3, a protein characteristic of Treg cells was studied , since it could potentially be influenced by the TGFb isoform levels. c) In an other group of patients the protein Activin A (ELISA), which has also been associated with either fibrosis or with regeneration of hepatocytes was evaluated. The effect of Octreotide in the levels of Activin A was also studied. Since few information exist about the origin of Activin A, in this part we studied the localization of the protein in non-parenchymal cells of the rat liver. Kupffer cells and hepatic stellate cells from were isolated and the expression of Activin A and the effect of Octreotide were evaluated using a semiquantitative PCR. d) Finally, serum levels and the effect of Octreotide on metalloproteases (MMPs) and the metalloprotease inhibitor TIMP1 was also evaluated by ELISA. ................

Η ηπατική ίνωση είναι ένα δυναμικό φαινόμενο η πρόοδος του οποίου εξαρτάται από την ενεργοποίηση των αστεροειδών κυττάρων του ήπατος. Η παραγωγή θεμέλιας ουσίας υπόκειται στην επίδραση…

Subjects/Keywords: Ίνωση ήπατος; Σωματοστατίνη; Λεπτίνη; Λαμινίνη; ΚΟΛΛΑΓΟΝΟ IV; Ακτιβίνη Α; Liver fibrosis; Somatostatin; Leptin; Laminins; Collagen IV; Activin A; TGFb

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Βουμβουράκη, . �. (2010). Ο ρόλος της οκτρεοτίδης ως αντιϊνωτικού παράγοντα σε ασθενείς με χρόνια ηπατοπάθεια. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/25020

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Βουμβουράκη, Αργυρώ. “Ο ρόλος της οκτρεοτίδης ως αντιϊνωτικού παράγοντα σε ασθενείς με χρόνια ηπατοπάθεια.” 2010. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed January 20, 2021. http://hdl.handle.net/10442/hedi/25020.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Βουμβουράκη, Αργυρώ. “Ο ρόλος της οκτρεοτίδης ως αντιϊνωτικού παράγοντα σε ασθενείς με χρόνια ηπατοπάθεια.” 2010. Web. 20 Jan 2021.

Vancouver:

Βουμβουράκη �. Ο ρόλος της οκτρεοτίδης ως αντιϊνωτικού παράγοντα σε ασθενείς με χρόνια ηπατοπάθεια. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2010. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/10442/hedi/25020.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Βουμβουράκη �. Ο ρόλος της οκτρεοτίδης ως αντιϊνωτικού παράγοντα σε ασθενείς με χρόνια ηπατοπάθεια. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2010. Available from: http://hdl.handle.net/10442/hedi/25020

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Oxford

21. Robertson, Ian Butler. An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction.

Degree: PhD, 2012, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932

► Many studies have demonstrated a connection between the fibrillin matrix and TGFβ signalling, but at present the mechanistic basis for this link is unclear. An… (more)

▼ Many studies have demonstrated a connection between the fibrillin matrix and TGFβ signalling, but at present the mechanistic basis for this link is unclear. An interaction between the C-terminus of Latent TGFβ Binding Protein 1 (LTBP1) and the N-terminus of fibrillin1 has previously been identified, and may have the potential to directly link the fibrillin matrix to TGFβ signalling. To investigate the structural basis for this interaction, several multi-domain fragments of fibrillin1 and LTBP1 were expressed prokaryotically and refolded in vitro. After initial characterisation to confirm folding, the structure, dynamics, and interdomain interactions of these fragments were investigated in more detail using NMR techniques. Domains in both LTBP1 and fibrillin1 appear to demonstrate folds consistent with homologous structures, and while the LTBP1 C-terminal cbEGF14-TB3-EGF3-cbEGF15 region contains many flexible linkers and few interdomain interactions, the fibrillin1 EGF2-EGF3-hyb1-cbEGF1 region appears rigid, with interfaces forming between all domains present. SPR studies were used to demonstrate binding between distinct LTBP1 and fibrillin fragments, suggesting interactions between multiple domains are involved in the LTBP1-fibrillin1 interaction. The binding sites involved were then mapped to specific residues using HSQC titration studies, and structural models for the LTBP1-fibrillin1 interaction were generated based on these data. Predictions from these models were used to target residues for site-directed mutagenesis, based on their potential involvement in salt bridges, and when certain residues were replaced with those of opposite charge, reductions in binding could be seen in the SPR assay. These key residues were consistent with a particular model of the LTBP1-fibrillin1 interaction, as derived from the HSQC titration data. The conservation of potential binding site residues through deuterostome evolution also supports an important biological role for the LTBP-fibrillin interaction.

Subjects/Keywords: 572; Medical sciences; Biology (medical sciences); Cardiovascular disease; Physiology; Extracellular matrix; Biochemistry; structural biology; fibrillin; Latent TGF beta binding protein; marfan syndrome; transforming growth factor beta; TGFbeta; TGFb; nuclear magnetic resonance; surface plasmon resonance; microfibril; fibrillin 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Robertson, I. B. (2012). An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932

Chicago Manual of Style (16^th Edition):

Robertson, Ian Butler. “An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction.” 2012. Doctoral Dissertation, University of Oxford. Accessed January 20, 2021. http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932.

MLA Handbook (7^th Edition):

Robertson, Ian Butler. “An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction.” 2012. Web. 20 Jan 2021.

Vancouver:

Robertson IB. An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction. [Internet] [Doctoral dissertation]. University of Oxford; 2012. [cited 2021 Jan 20]. Available from: http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932.

Council of Science Editors:

Robertson IB. An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction. [Doctoral Dissertation]. University of Oxford; 2012. Available from: http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932

22. Moussavi Nik, Seyed Ali. FoxF genes in development and disease.

Degree: 2014, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/35534

► Forkhead transcription factors of the FoxF group are important during embryonic de-velopment, and mutation of either of the members, Foxf1 and Foxf2, has fatal conse-quences.… (more)

▼ Forkhead transcription factors of the FoxF group are important during embryonic de-velopment, and mutation of either of the members, Foxf1 and Foxf2, has fatal conse-quences. In this thesis, I present our recent findings about the mechanism of action of FoxF genes in development and disease. Haploinsufficiency for FOXF1 in humans causes alveolar capillary dysplasia with mis-alignment of pulmonary veins (ACDMPV), a rare lethal congenital disorder with incom-plete penetrance. We report a new ACDMPV case and define the genomic rearrangement which consists of a pericentric inversion on chromosome 16 (p11.2q24.1), which dis-rupts the FOXF1 5’-flanking region 134 kb upstream of the first exon. We further use this information in combination with chromatin modification data from the ENCODE data set to predict the extent of the FOXF1 regulatory domain and the critical genomic regions for ACDMPV. Gastrointestinal cancer, which is the result of uncontrolled proliferation of intestinal stem cells, is one of the most prevalent causes of death in the West. We show that Foxf2 regulates the number of intestinal stem cells and the proliferation rate in adult mouse intestine, with consequences for initiation and growth of intestinal tumors. Foxf2 limits the size of the stem cell niche by activating the expression of the extracellular Wnt inhib-itor Sfrp1 in mesenchymal cells surrounding the crypts of Lieberkühn. During this work we also developed a novel method for separation of intact intestinal epithelium from mesenchyme. Cleft palate is a common congenital malformation, associated with many genetic al-terations and environmental teratogens. Loss of Foxf2 results in cleft palate in mouse. We found that the cleft palate is the result of reduced proliferation and decreased extra-cellular matrix production in the neural crest-derived palatal shelf mesenchyme at a critical stage of palatal formation. The mechanistic basis appears to be a diminished Tgfβ signaling, and decreased expression of integrins required for activation of latent Tgfβ.

Subjects/Keywords: FOXF1; Sfrp1; LGR5+stem cells; Tgfb; Wnt signaling; ECM; Intact intestinal epithelium; Foxf2; ACDMPV

…Smad5, or Smad8, which heterodimerize with the common Tgfb/Bmp…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Moussavi Nik, S. A. (2014). FoxF genes in development and disease. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/35534

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Moussavi Nik, Seyed Ali. “FoxF genes in development and disease.” 2014. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 20, 2021. http://hdl.handle.net/2077/35534.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Moussavi Nik, Seyed Ali. “FoxF genes in development and disease.” 2014. Web. 20 Jan 2021.

Vancouver:

Moussavi Nik SA. FoxF genes in development and disease. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2014. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/2077/35534.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Moussavi Nik SA. FoxF genes in development and disease. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2014. Available from: http://hdl.handle.net/2077/35534

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

23. Bandyopadhyay, Tirthankar. Defining the Effects of GDF-2 on TGF_B Signaling in Tumorigenic Epithelial Cells.

Degree: MS, Chemistry and Biochemistry, 2015, University of South Carolina

URL: https://scholarcommons.sc.edu/etd/3247

► Cancer cells can be viewed as such cells, which have disrupted/aberrant signaling pathways for maintaining cellular homoeostasis. Identifying such altered signaling mechanisms can help… (more)

Subjects/Keywords: Chemistry; Physical Sciences and Mathematics; Tumorigenic epithelial cells; GDF-2; TGFb

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bandyopadhyay, T. (2015). Defining the Effects of GDF-2 on TGF_B Signaling in Tumorigenic Epithelial Cells. (Masters Thesis). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/3247

Chicago Manual of Style (16^th Edition):

Bandyopadhyay, Tirthankar. “Defining the Effects of GDF-2 on TGF_B Signaling in Tumorigenic Epithelial Cells.” 2015. Masters Thesis, University of South Carolina. Accessed January 20, 2021. https://scholarcommons.sc.edu/etd/3247.

MLA Handbook (7^th Edition):

Bandyopadhyay, Tirthankar. “Defining the Effects of GDF-2 on TGF_B Signaling in Tumorigenic Epithelial Cells.” 2015. Web. 20 Jan 2021.

Vancouver:

Bandyopadhyay T. Defining the Effects of GDF-2 on TGF_B Signaling in Tumorigenic Epithelial Cells. [Internet] [Masters thesis]. University of South Carolina; 2015. [cited 2021 Jan 20]. Available from: https://scholarcommons.sc.edu/etd/3247.

Council of Science Editors:

Bandyopadhyay T. Defining the Effects of GDF-2 on TGF_B Signaling in Tumorigenic Epithelial Cells. [Masters Thesis]. University of South Carolina; 2015. Available from: https://scholarcommons.sc.edu/etd/3247

24. Yun, James Jungwon. LKB1/AMPK Pathway as a Potential Target for Cancer Treatment and its Role in TGFB Signaling.

Degree: 2014, University of Toronto

URL: http://hdl.handle.net/1807/67321

►

Although the “Warburg Effect” was reported >50 years ago, in recent years, there has been much greater appreciation for the importance of understanding perturbations in… (more)

▼

Although the “Warburg Effect” was reported >50 years ago, in recent years, there has been much greater appreciation for the importance of understanding perturbations in metabolic pathways of cancer cells. Among many key players in cancer metabolism, liver kinase B1 (LKB1) and AMP-activated protein kinase (AMPK) have been under the spotlight because they function as metabolic switches that regulate several biosynthetic pathways in response to nutrient availability. One of the most highlighted metabolic pathways regulated by AMPK is the mammalian target of rapamycin (mTOR) pathway that controls protein synthesis in cells. Since AKT/PKB activates mTOR to antagonize the effect of AMPK-mediated inhibition of cell proliferation, the balance between AMPK and AKT activation may determine the overall direction of cellular metabolism favoring either growth arrest or proliferation. The first part of this thesis investigated the possible synergy between Metformin-mediated activation of AMPK and MK-2206-mediated inhibition of AKT on cell growth inhibition in vitro. Furthermore, the possibility of using AKT activation level as a molecular marker to predict in vitro sensitivity to Metformin for any given cell line was tested. In the second part, it was hypothesized that LKB1/AMPK pathway may be involved in transforming growth factor β (TGFΒ)-mediated inhibition of cell proliferation as LKB1/AMPK pathway is central in the regulation of general cellular metabolism to inhibit cell proliferation. Consequently, defects in LKB1/AMPK pathway, which occur in a significant portion of lung adenocarcinoma patients, may lead to impaired TGFΒ responses in cancer cells. Therefore, the mechanism of how LKB1 deletion affects the TGFΒ signaling in cancer cells was investigated using three different LKB1-modulated lung cancer cell lines. This study showed that 1) Metformin and MK-2206 exhibit synergy in inhibiting cell growth in vitro, but neither phospho-AKT nor two downstream targets of mTOR signal (phospho-P70S6K and phospho-S6RP) are good predictors of Metformin sensitivity, and that 2) LKB1/AMPK pathway is important for proper TGFΒ signaling and regulates the expression of TGFΒ1, TGFΒ2, TGFΒR2 and SMAD3 as well as the linker phosphorylation of SMAD2. From these results, it was concluded that LKB1/AMPK pathway may play multiple roles in oncogenesis by regulating cell growth in conjunction with AKT/mTOR pathway and by interacting with TGFB signaling.

PhD

Advisors/Committee Members: Tsao, Ming-Sound, Laboratory Medicine and Pathobiology.

Subjects/Keywords: LKB1; STK11; AMPK; Metformin; MK-2206; AKT; mTOR; Cancer Metabolism; Drug Synergy; Combination Treatment; Tumor Suppressor; TGFB; Lung Cancer; Cancer; 0307; 0379

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yun, J. J. (2014). LKB1/AMPK Pathway as a Potential Target for Cancer Treatment and its Role in TGFB Signaling. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/67321

Chicago Manual of Style (16^th Edition):

Yun, James Jungwon. “LKB1/AMPK Pathway as a Potential Target for Cancer Treatment and its Role in TGFB Signaling.” 2014. Doctoral Dissertation, University of Toronto. Accessed January 20, 2021. http://hdl.handle.net/1807/67321.

MLA Handbook (7^th Edition):

Yun, James Jungwon. “LKB1/AMPK Pathway as a Potential Target for Cancer Treatment and its Role in TGFB Signaling.” 2014. Web. 20 Jan 2021.

Vancouver:

Yun JJ. LKB1/AMPK Pathway as a Potential Target for Cancer Treatment and its Role in TGFB Signaling. [Internet] [Doctoral dissertation]. University of Toronto; 2014. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1807/67321.

Council of Science Editors:

Yun JJ. LKB1/AMPK Pathway as a Potential Target for Cancer Treatment and its Role in TGFB Signaling. [Doctoral Dissertation]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/67321

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Open Access Theses and Dissertations