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Dissertations / Theses on the topic 'Fibroblast growth factors'

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Published: 4 June 2021

Last updated: 25 July 2024

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1

Patel, Ambreen. "Fibroblast growth factors and retinal cell genesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0025/MQ48033.pdf.

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2

Detvisitsakun, Chanitchote. "Functional characterization of a Baculovirus fibroblast growth factor." Diss., Manhattan, Kan. : Kansas State University, 2006. http://hdl.handle.net/2097/239.

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3

Harmer, N. J. "Structural studies of fibroblast growth factors and their receptors." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603723.

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Recent crystal structures have suggested two models for the complex between FGFs, FGF receptors (FGFRs) and the proteoglycan heparin that mediates signalling, and have provided insight into how FGFs show differing affinities for the range of FGFRs. I have examined complexes of FGF, FGFR and heparin by size-exclusion chromatography, analytical ultracentrifugation and mass spectrometry. This analysis suggests that both of the crystal structures faithfully represent the state of the molecules in solution. From this, I conclude that the origin of the difference in the two models lies in the preparation of the complexes, and propose a resolution of the controversy. Using longer heparan sulphate fragments, I have observed larger complexes with FGF and FGFR. Further study of these complexes provides compelling evidence that these larger complexes correspond to a dimer of the FGF-FGFR complexes previously observed. These larger complexes give an insight into how higher order complexes of FGFs and FGFRs may form on the cell surface. FGF19, one of the most divergent human FGFs, is unique in binding solely to one receptor, FGFR4. Having cloned the human FGF19 gene, I devised a strategy of expression and purification to provide sufficient quantities of pure FGF19 for crystallisation. I have used molecular replacement to solve the crystal structure of FGF19 at 1.3 A resolution. The structure shows that two novel disulphide bonds found in FGF19, one of which appears to be conserved among several of the other FGFs, stabilise extended loops. The key heparin binding loops of FGF19 have radically different conformations and charge patterns, compared to other FGFs, correlating with the unusually low affinity of FGF19 for heparin. A model for the complex of FGF19 with FGFR4 demonstrates that sequences unique to both FGF19 and FGFR4 are key to the formation of the complex. The structure therefore offers a clear explanation for the unusual affinity of FGF19 for FGFR4 alone.

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4

Ding, Su Sin. "Fibroblast growth factors in gastrointestinal development, homeostasis and injury." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5497.

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Fibroblast growth factors (FGFs) and their receptors (FGFRs) are essential for controlling cell growth and proliferation, angiogenesis, wound healing and tumourigenesis. In mammals, there are twenty-three FGFs and five FGFRs, with each FGFR having different ligand binding specificities. FGFs are thought to act in a paracrine manner, in which they are secreted by one cell and activate FGFRs on another cell type, and such interaction helps to establish the fundamental crosstalk between epithelium and mesenchyme during development, homeostasis and tumourigenesis. This thesis aims to investigate the requirement of FGFR2-isoform IIIb (Fgfr2b) and one of its ligands, Fgf10, in gastrointestinal (GI) development, homeostasis and injury, using loss-of-function animal models. Fgfr2b-/- and Fgf10-/- exhibit similar multi-organ defects, including intestinal atresia. While caecal and colonic atresia have been previously described, the mechanism of duodenal atresia and the role of Fgf signalling in duodenal development have not been fully established. We demonstrate that absence of Fgfr2b or Fgf10 leads to decreased tissue proliferation and increased apoptosis in the duodenum, contributing to duodenal atresia. These mutants also develop gastric heterotopia in the rostral duodenum due to loss of gastric-intestinal boundary specification. In addition, we demonstrate reduced expression of Wnt targets Tcf1 and Tcf4 in the small intestine, with corresponding downregulation of Lgr5, an intestinal stem cell marker, and Cdx1, a homeobox gene involved in anterior-posterior patterning. We show by in vitro that Fgf10-Fgfr2b signalling is able to regulate Tcf4 expression via the Grb2/Sos/Ras/MAPK pathway. In order to study the requirement of Fgfr2b in intestinal homeostasis and injury, we crossed a transgenic line bearing a progesterone antagonist (RU486)-dependent Cre recombinase (A33-CrePR) expressed under the control of the intestinal-specific A33 antigen promoter, with an existing conditional Fgfr2b line. Following RU486 administration with/without administration of dextran sodium sulphate (DSS) thereafter to induce ulcerative colitis (UC), the A33-CrePR+/Fgfr2bflox/flox targeted Fgfr2b ablation with high efficiency across the small and large intestine. We demonstrate that significant downregulation of Fgfr2b does not affect intestinal homeostasis, but significantly increases the susceptibility of colonic epithelium to UC and delays wound healing, contributed by reduced epithelial proliferation. In order to study the requirement of Fgfr2b in gastric homeostasis, we characterised two stomach-specific minimal promoters for trefoil factor 1 (Tff1) and H+K+-ATPase (Atp4b) to generate two inducible Cre recombinase (CreERT2) lines. Gastric surface mucous cells and acidproducing parietal cells express Tff1 and Atp4b respectively, as well as Fgfr2b. We demonstrate by in vitro that Atp4b nucleotide -1,035bp to +24 bp and Tff1 nucleotide -641 bp to +28 bp are optimal for driving Cre expression in the mouse stomach. Thus, our novel data provides evidence that Fgfr2b and Fgf10 are required for normal duodenal morphogenesis and differentiation, and Fgfr2b confers protection against DSS-induced colonic injury and promotes wound repair.

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5

Moenner, Michel. "Étude du mécanisme d'action des facteurs de croissance "Fibroblast Growth Factors" (FGF)." Paris 12, 1988. http://www.theses.fr/1988PA120010.

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Pour les deux types cellulaires etudies, il apparait que le signal mitogene induit par la formation du complexe fgf-recepteurs est independant de l'activation du cycle des polyphosphoinositides et de l'activation de la proteine kinase c

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6

Moenner, Michel. "Etude du mécanisme d'action des facteurs de croissance "fibroblast growth factors", FGF." Grenoble 2 : ANRT, 1988. http://catalogue.bnf.fr/ark:/12148/cb376165817.

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7

Scarpa, Richard C. "Neurotensin potentiates the proliferative effects of growth factors in human embryonic lung fibroblasts /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2004.

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Thesis (Ph.D.)--Tufts University, 2004.
Adviser: David E. Cochrane. Submitted to the Dept. of Biology. Includes bibliographical references (leaves 137-165). Access restricted to members of the Tufts University community. Also available via the World Wide Web;

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8

Abud, Helen E. "Examination of methods for the study of FGFs during mouse development." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260765.

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9

Vidyasagar, Rishma. "Characterisation of a suitable surface for the study of FGF : oligosaccharide interactions." Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288274.

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10

Yeoh, Joyce Siew Gaik. "Regulatory role of fibroblast growth factors on hematopoietic stem cells." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2007. http://irs.ub.rug.nl/ppn/299000842.

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11

Pulkkinen, Mari-Anne. "Role of epidermal and fibroblast growth factors in pancreatic development." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/haart/vk/pulkkinen/.

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12

Braithwaite, Vickie. "Predictors of rickets in the Gambia : fibroblast growth factor-23." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607859.

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13

Rowntree, Sharon R., and University of Lethbridge Faculty of Arts and Science. "Basic fibroblast growth factor in the injured brain." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 1995, 1995. http://hdl.handle.net/10133/38.

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Basic fibroblast growth factor (bFGF) has been implicated in the brain's trophic response to injury. This thesis examined the effects of endogenous bFGF on brain plasticity and recovery of behavioral function following cortical injury in adult rats. The first experiment investigated the post-lesion time course of the astrocytic expression of bFGF. Subsequent experiments examined the effects of injury-induced bFGF on neuroonal morphology, cortical morphology, and post-lesion behavioral deficits. Following motor cortex injury, endogenous bFGF prevented neuritic degeneration in layer V pyramidal neurons in Zilles' area Fr2 and promoted recovery of function in the Whishaw Reaching Task. Housing rats in an enriched environment prior to cortical injury enhanced the expression of bFGF but did not increase cortical thickness nor reduce post-lesion behavioral deficits (relative to laboratroy-housed rats). Collectively, these experiments indicate that injury-induced bFGF plays a role in potentiating recovery from brain damage. This implies that bFGF may be beneficial as a treatment following brain injury.
x, 123 p. ; 28 cm.

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14

Chen, Pei-Yu. "Fibroblast Growth Factor Receptor-1 (FGFR1) in Vascular Smooth Muscle Cell Phenotypic Switch." Fogler Library, University of Maine, 2009. http://www.library.umaine.edu/theses/pdf/ChenPY2009.pdf.

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15

Waite, Wendy Lou, and University of Lethbridge Faculty of Arts and Science. "Basic fibroblast growth factor enhances recovery in rats." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2003, 2003. http://hdl.handle.net/10133/208.

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This thesis examined the role of exogenous basic fibroblast growth factor (FGF-2) in stimulating recovery after early cortical injury. Rats with medial prefrontal cortex (MFC), posterior parietal cortex (PPC), or sham lesions at postnatal day 3 (P3) received one of three variations of FGF-2 treatment: postnatal FGF-2 that was either pre-mixed or prepared daily, or prenatal FGF-2, and tested in adulthood. Behavioral tests used were: 1) the Morris Water task and, 2) the Whishaw Tray Reaching task. The level of functional recovery attained was dependent on FGF-2 preparation and the developmental period. MFC lesion rats showed good recovery but there was a differntial effect of pre and postnatal FGF-2 that appeared to be related to task. PPC rats showed greater recovery after postnatal rather than prenatal treatment. Anatomical changes were restricted to groups with relatively good functional recovery. These findings suggest a multifunctional role of FGF-2 in the injured brain.
xvi, 223 leaves : ill. ; 29 cm.

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16

Maker, Garth Lucas. "Regulation of surfactant production by fetal type II pneumocytes and characterization of fibroblast-pneumocyte factor /." Access via Murdoch University Digital Theses Project, 2007. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20080430.141113.

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17

Yu, Bei. "Basic fibroblast growth factor as a therapeutic target for chemosensitization in colorectal cancer." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1142882177.

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18

Smith, Simone Marsha-Lee. "The proteoglycan perlecan regulates long bone growth through interactions with developmental proteins in the growth plate." [Tampa, Fla.] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0002155.

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19

Tanenbaum, Michael David. "Control of angiogenic responses through an evolutionary conserved sequence of fibroblast growth factor." Thesis, Georgia Institute of Technology, 2003. http://hdl.handle.net/1853/20209.

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20

Walsh, Colin T. "Molecular pharmacodynamics of chemotherapy fibroblast growth factor (FGF) inhibitors as chemosensitizers /." Connect to resource, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1126212295.

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21

Gallego-Llamas, Jabier. "Retinoic acid and Fibroblast Growth Factors during segmentation and somite formation." Université Louis Pasteur (Strasbourg) (1971-2008), 2007. http://www.theses.fr/2007STR13249.

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Au cours de la somitogénèse, l’action combinée d’un oscillateur moléculaire et la progression d’un front de détermination conduit à la formation périodique et synchronisée des somites. La régulation de la somitogénèse est sous le contrôle de plusieurs voies de signalisation dont les voies Notch, Wnt et Fgf. Récemment nous avons montré l’importance de l’acide rétinoïque (AR) dans cette cascade pour le positionnement correct des frontières somitiques de la synchronisation gauche/droite des oscillations moléculaires. L’asymétrie induite par la déficience en AR semble entre autre passer par la régulation du gène Fgf8. De plus, l’analyse par time-lapse d’embryons de zebrafish déficients en AR a montré une dérégulation progressive de la formation des somites. Enfin, l’analyse de gènes Hox et de gènes Cdx a montré la nécessité d’une régulation spatio-temporelle dans la production de l’AR et du Fgf8 pour la formation correcte d’une structure squelettique
Somitogenesis is a process that can be used as a model of body segmentation. The actual model used to describe segmentation is based on a model called the “Clock and Wavefront”. This model is based on a clock made by oscillating gene expression and on a wavefront determined by the gradient of specific genes. This mechanism allows the symmetrical and dynamic formation of the somites that will give rise to several structures among which the axial skeleton. We show that the absence of RA induce asymmetrical somite formation and due to at least the asymmetrical expression of Fgf8 deficiency. Moreover we show that there is a progressive deregulation in the formation of the somites by looking by a timelapse method in a Zebrafish RA-deficiency model. Finally, the analyses of the Hox genes and the Cdx genes demonstrate the necessity to have a correct spatio-temporal production of RA and Fgf8 to manage to form a correct body plan

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22

陸梅 and Mei Lu. "Allogeneic bone grafts mixed with basic fibroblast growth factor: a cellular and molecular study." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B29866340.

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23

Seet, Li Fong. "Characterization of the biological properties of FGF-9." Thesis, University of Oxford, 1996. http://ora.ox.ac.uk/objects/uuid:a46cee92-c179-4d22-b27b-0e67c3c85a37.

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The fibroblast growth factor family of polypeptides currently consists of nine structurally-related members. Cloning of the mouse homologue of the latest reported member of the family, FGF-9, is described in this study. Mouse Fgf9 exhibits a high level of sequence conservation with the human, rat and Xenopus counterparts. Of note is the lack of a hydrophobic signal peptide at the N-terminus of the coding sequence. The protein, however, appeared to be secreted by producer cells since a significant quantity of the protein could be purified from the culture supernatant of transfected cells. Members of the FGF family are known to bind to cell surface tyrosine kinase receptors (FGFRs) to elicit a variety of physiological responses. These receptors themselves form a family of four structurally-related tyrosine kinases and each FGF member commonly has the ability to bind several members of the FGFR family. By using in vitro plate binding assays, FGF-9 is shown in this study to bind specifically to two FGFR members: FGFR2b and FGFR3c. To further study the potential functional role of FGF-9, its expression pattern in the mouse embryo was examined by both RNase protection and RNA in situ hybridization analyses. The transcript was detected in a variety of embryonic tissues: the germinal epithelium of the central nervous system, the mesonephric cords, the somites, the gut primordia and the developing eye and ear, suggesting that the gene may have multiple roles during development. In addition, the potential involvement of FGF-9 in mediating adult brain functions was examined by double RNA in situ hybridization analysis of the distribution of both Fgf9 and Fgfr3 transcripts in the adult mouse brain. Most apparent areas of co-localization are the olfactory bulb and cerebral cortex. The two transcripts are also shown to have distinct distribution patterns in the cerebellum.

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24

Zamora, Brian G. "Functions of Rx in early vertebrate ocular development." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10830.

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Thesis (Ph. D.)--West Virginia University, 2009.
Title from document title page. Document formatted into pages; contains x, 148 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 136-148).

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25

Nash, Gordon W. "Characterization of fibroblast growth factor receptor type I isoforms in Xenopus laevis embryonic development /." Internet access available to MUN users only, 2003. http://collections.mun.ca/u?/theses,167327.

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26

Schuschereba, Steven Theodore. "An investigation of factors modulating wound healing after laser damage to the retina." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251783.

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27

Pierce, Paul Randall 1951. "Control of fibroblast contamination in primary rat skeletal muscle cell cultures: Effects of an epidermal growth factor linked cytotoxin." Thesis, The University of Arizona, 1988. http://hdl.handle.net/10150/276812.

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The in vitro study of muscle cell growth is hampered by the presence of non-muscle cells, particularly fibroblasts. The heterobifunctional cross-linking agent, N-succinimidyl 3-(2-pyridyldithio) propionate (SPDP) has been used to create a novel "toxic growth factor" to address the problem. Epidermal growth factor (EGF), which stimulates fibroblast but not satellite cell proliferation, was conjugated via SPDP to a potent ribosome inhibitor, pokeweed antiviral protein (PAP). By preferentially binding to fibroblasts, it was hoped that EGF-PAP could cytotoxically eliminate fibroblasts from primary cultures of rat skeletal muscle satellite cells. While EGF-PAP did prove to be a fibroblast cytotoxin, it could not completely eliminate them from cell cultures. Low dose-time exposures improved the ratio of multinucleated cells to mononucleated cells (percent fusion) by up to 66% over controls, but increased concentrations, or durations of EGF-PAP treatment, proved detrimental to satellite cell growth and/or differentiation.

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28

Ryan, Paula. "Characterization of the FGF receptor signaling complex in Xenopus laevis during early embryonic development /." St. John's, NF ; [s.n.], 1999.

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29

Butt, Richard Philip. "Effect of mechanical forces and polypeptide growth factors on cardiovascular fibroblast function." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363055.

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30

Baradji, A. "Interactions of fibroblast growth factors with glycosaminoglycan brushes and the pericellular matrix." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3019050/.

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31

Martin, Christopher School of Biomedical Engineering UNSW. "Investigation of exogenous growth factors; platelet derived growth factor, insulin-like growth factor binding protein and fibroblast growth factor, and their influence on in vivo bone repair." Awarded by:University of New South Wales. School of Biomedical Engineering, 2006. http://handle.unsw.edu.au/1959.4/30405.

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This research investigated if exogenous growth factors (GFs), in particular platelet derived growth factor (PDGF), has an in vivo effect on the healing response of normal healthy bone. The research was orientated to study whether a clinical beneficial effect could be demonstrated. To achieve this two animal models were utilised, namely, a rabbit tibial osteotomy model and an ovine tibial defect and porous implant ingrowth model. The rabbit model comprised of a unilateral V-shaped tibial osteotomy, stabilised with an absorbable intramedullary pin and figure-of-eight tension band suture, with a 3 week survival period. The GFs tested in this model were 3 concentrations of PDGF, a single dose of insulin-like growth factor binding protein (IGF-BP) and a combination of the two. Each osteotomy was injected with a single bolus of collagen (control) or collagen containing GF (treatment) during surgery. After sacrifice tibiae were CT-scanned in situ, harvested and subject to 4-point bend testing. The callus, underlying bone and contralateral bone's greyscales and mechanical testing results were used for comparative analysis. The ovine model consisted of implanting 6 small rectangular shaped titanium alloy porous implants and one empty defect bilaterally in sheep's tibiae, for 4 and 6 weeks. The sheep were injected with tetracycline bone marker at 2 week intervals. The model's characteristics and any positional effects were initially investigated. Followed by an investigation into the influence of various exogenous GFs on the healing response and ingrowth characteristics of bone into the porous implants. The GFs investigated were PDGF, IGF-BP and fibroblast growth factor impregnated into the porous implants in a collagen carrier. Comparative analysis was done on results from 3-point bend testing of the bone/implant interface, image analysis to quantify percentage of bone, from scanning electron microscopy images of implant sections and confocal microscopy images of tibial defect sections. Analyses indicate that the GFs investigated have a direct and quantifiable positive in vivo effect. The more significant finding is that the growth factors have a potent systemic effect. These results were confirmed by both the sheep porous bone plug model and the rabbit tibial osteotomy model used within this research.

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32

Drugan, Caroline S. "The role of fibroblast growth factors and their receptors in human oral carcinogenesis." Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389231.

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33

McCabe, Kathryn Leigh. "The transition from progenitor cell to neuron : fibroblast growth factors and their role in retinal ganglion cell neurogenesis /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/10640.

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34

Bhatnagar, Sushant. "Fibroblast growth factor-19 a novel factor that inhibits hepatic fatty acid synthesis /." Morgantown, W. Va. : [West Virginia University Libraries], 2008. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=6060.

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Thesis (Ph. D.)--West Virginia University, 2008.
Title from document title page. Document formatted into pages; contains ix, 86 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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35

Kreuger, Johan. "Decoding Heparan Sulfate." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5161-6/.

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36

Magnusson, Peetra. "Fibroblast Growth Factor Receptor-1 Function in Vasculo- and Angiogenesis." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5824.

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37

Song, Jihwan. "Cloning, expression and biological activity of fibroblast growth factors in early Xenopus development." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307020.

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38

Mehta, Piyush Bachoolal. "The roles of fibroblast growth factors and their receptors in human prostate cancer." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311115.

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39

Dorkin, Trevor John. "The role of fibroblast growth factors in the pathogenesis of human prostate cancer." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366585.

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40

Heer, Rakesh. "Characterisation of fibroblast growth factors in differentiation and carcinogenesis of the human prostate." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423723.

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41

Bresnick, Janine Nicola. "The fibroblast growth factors and their receptors in mammary gland development and malignancy." Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307597.

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42

Wang, Jie. "Broad-Spectrum Protection Against Chemotherapy-Induced Alopecia by Acidic and Basic Fibroblast Growth Factors." The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1111433922.

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43

Knights, Victoria E. E. "Tumour cell responses to novel fibroblast growth factor receptor (FGFR) tyrosine kinase inhibitors." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608393.

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44

Boulle, Nathalie. "Analyse du système des insulin-like growth factors (IGF) et du fibroblast growth factor-2 (FGF-2) dans la tumorigenèse corticosurrenalienne." Paris 11, 2000. http://www.theses.fr/2000PA11T006.

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Dans les tumeurs corticosurrénaliennes, des anomalies de la région 11p15 et une surexpression du gène d'IGF-11 sont contemporaines de l'acquisition du phénotype malin. Nous montrons que la surexpression du gène IGF-11 dans les tumeurs corticosurrénaliennes malignes s'accompagne d'une traduction efficace de la protéine, majoritairement sous forme de précurseurs d'IGF-11. Ces mêmes tumeurs surexpriment de manière spécifique IGFBP-2, protéine de liaison des IGF fréquemment associée à la prolifération tumorale. La caractérisation de la lignée H295R, dérivée d'un carcinome surrénalien, montre que celle-ci surexprime IGF-11 et IGFBP-2 et constitue un bon modèle in vitro d'ét•ude de la tumorigénèse corticosurrénalienne. Cette lignée a permis de démontrer qu'IGF-11 était impliqué dans la prolifération des cellules tumorales corticosurrénaliennes via le récepteur de type 1 des IGF. L'intérêt de I'IGFBP-2 plasmatique en tant que marqueur circulant des tumeurs corticosurrénaliennes malignes a été évalué. Nous montrons que les taux d'IGFBP-2 plasmatique s'élèvent spécifiquement chez les patients porteurs de tumeurs malignes mais que cette élévation survient à lin stade avancé de la maladie (stade métastatique), indiquant la faible sensibilité d'IGFBP-2 et son intérêt limité comme marqueur des carcinomes surrénaliens. Les effets de FGF-2 sur les cellules tumorales corticosurrénaliennes ont également été étudiés. Nos résultats montrent que FGF-2 a un effet prolifératif sur les cellules H295R mais que paradoxalement, il inhibe l'expression du système des IGF par ces cellules. L'inhibition d'IGFBP-2 se fait au niveau transcriptionnel, alors que celle d'IGF-11 est post-transcriptionnelle, par inhibition de la maturation des précurseurs d'IGF-11. Ainsi, si IGF-11 a un rôle indiscutable au stade tardif de la tumorigénèse corticosurrénalienne, différents facteurs sont susceptibles de moduler son expression (FGF-2) ou son activité (IGFBP-2) au sein du tissu tumoral
Ln adrenocortical tumors, malignant phenotype is associated with abnormalities at the 11p15 locus and overexpression of the IGF-11 gene. Here, we show that IGF-11 mRNA is efficiently translated and that malignant adrenocortical tumors contain large amounts of IGF-11 protein, mainly in its prohormone form. The same tumors exhibit a high content in IGFBP-2 protein, an IGFBP being frequently expressed in tumor cells. The H295R cell line, which is derived from a human adrenal carcinoma, express high levels of both IGF-11 and IGFBP-2 and represents a suitable in vitro model to study adrenocortical tumorigenesis. Using this cell line, we could demonstrate that IGF-11 is involved in the proliferation of adrenocortical tumor cells, after binding to the type 1 IGF receptor. The interest of plasma IGFBP-2 as a marker for adrenocortical carcinoma was evaluated. Our results show that high levels of IGFBP-2 are specifically detected in the plasma of patients with malignant adrenocortical tumors. However, the increase in IGFBP-2 levels occur at a late stage of tumor progression (metastatic stage). This indicates a poor sensitivity for plasma IGFBP-2, which may limit its interest as a tumor marker. We also studied the effects of FGF-2 on adrenocortical tumor cells. Our results indicate that FGF-2 is mitogenic for H295R cells, although it inhibits the expression of both IGF-11 and IGFBP-2 by these cells. The inhibition of IGFBP-2 expression occur at the transcriptional levels. Ln contrast, FGF-2 inhibits the secretion and the last steps of maturation of the IGF-11 precursor. Altogether, these results suggest that in malignant adrenocortical tumors, various factors may modulate the expression (FGF-2) or the effects (IGFBP-2) of IGF-11 on adrenocortical tumor cells

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Li, Yu. "Cloning and characterization of a cDNA encoding er1 , a novel developmentally regulated FGF response gene." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0030/MQ47427.pdf.

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Fletcher, Michael. "Network analysis of fibroblast growth factor receptor 2-regulated gene expression in breast cancer." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608087.

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Pazmany, Csaba C. "In Vitro analysis of FGF-23 induced gene expression." Link to electronic thesis, 2003. http://www.wpi.edu/Pubs/ETD/Available/etd-0114103-160205.

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Thesis (M.S.)--Worcester Polytechnic Institute.
Keywords: factor; FGF-23; phosphatonin; microarray; expression; phosphate; time; gene; RT-PCR; growth; fibroblast. Includes bibliographical references (p. 127-136).

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48

Quennell, Janette Henrietta, and n/a. "Molecular and cellular biology of FGF2 in human ovarian follicles." University of Otago. Department of Anatomy & Structural Biology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20061025.142115.

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Ovaries maintain and produce functional female gametes, oocytes, for fertilisation. Oocytes develop inside cellular assemblies, the ovarian follicles, before birth and can reside there for up to 50 years in the human. Despite recent inroads, the precise mechanisms of initial follicle recruitment and growth remain unclear. Although the pituitary gonadotrophins play a role in this developmental process, locally produced factors have been implicated strongly in initiation of follicle growth. It is known that fibroblast growth factor 2 (FGF2) is a powerful mitogen for follicular granulosa cells in culture and initial studies undertaken in this project were successful in detecting FGF2 gene expression in ovarian biopsies from fertile healthy women. To further elucidate which cells were expressing FGF2, laser microdissection was employed to isolate differentially staged follicle populations. Real-time RT-PCR was used to quantify mRNA in relation to follicle development. Decreasing levels of FGF2 expression were detected as follicles developed. Non-radioactive in situ hybridisation confirmed FGF2 mRNA localisation in granulosa cells of preantral follicles. FGF2 protein localisation was assessed with immunohistochemistry; two primary antibodies raised against different fragments of human FGF2 were used. Both antibodies detected FGF2 in the oocyte cytoplasm of putative non-growing follicles, whereas only one of the antibodies showed additional reactivity to the basement membrane region of these same follicles. These results suggest different isoforms of FGF2 may localise specifically to different cellular sites. Follicle stimulating hormone receptor (FSHR) gene expression was also investigated in follicles using laser microdissection, real-time RT-PCR and in situ hybridisation. FSHR mRNA was detected in all follicle populations, including the smallest putative non-growing follicles. Disparity to other published works was attributed to the position of primer annealing, and thus the ability to detect alternatively spliced transcripts. In conclusion, the work presented here provides evidence that FGF2 and FSHR are present in small follicles and that their actions may be stimulatory or inhibitory to initial follicle recruitment.

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Ge, Xuan, and 戈萱. "Fibroblast growth factor 21 as a key modulator of glucose uptake and lipolysis in adipocytes: molecular mechanismsand physiological implications." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hub.hku.hk/bib/B50434378.

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Fibroblast Growth Factor (FGF) 21 is a liver-derived endocrine factor with multiple metabolic effects on glucose and lipid homeostasis in animals. The adipose tissue has been proposed as a major target of FGF21, where it enhances glucose uptake and modulates lipolysis as well as thermogenesis. However, the molecular mechanisms underlying the pleiotropic effects of FGF21 in adipocytes and the physiological roles of FGF21 in regulating energy homeostasis remain poorly characterized. Therefore, the present study aimed to investigate: 1) the signal transduction pathway whereby FGF21 enhances glucose uptake in white adipocytes; 2) the role of FGF21 in lipolysis in both mouse and human white adipose tissues (WAT) and its underlying mechanisms involved; 3) the phenotypes of FGF21 knockout (KO) mice with respect to energy expenditure and adiposity under both standard chow and high fat diet. Key findings: 1. In vitro studies demonstrated that extracellular signal-regulated kinases (ERK1/2) play an obligatory role in mediating FGF21-induced upregulation of glucose transporter-1 (GLUT1) expression and hence elevation of glucose uptake in 3T3-L1 adipocytes. 2. Chromatin immunoprecipitation assay revealed that Serum Response Factor (SRF) and ETS-like protein-1 (Elk-1), the two transcription factors which are known as the downstream targets of ERK1/2, were recruited to the endogenous GLUT1 promoter in adipocytes. A conserved binding motif for these two transcription factors was also identified in the GLUT1 promoter responsive to FGF21 stimulation in 3T3-L1 adipocytes by site-directed mutagenesis and luciferase assay. 3. In WAT of diet-induced obese mice, FGF21-evoked downstream signaling events, including the phosphorylation of ERK1/2 and SRF/Elk-1, the upregulation of GLUT1, and the increased glucose uptake, were markedly blunted compared to lean controls, suggesting the existence of “FGF21 resistance” in obesity. 4. In vivo and ex vivo studies on fasted wild type and FGF21 KO mice demonstrated that FGF21 acutely suppressed basal and forskolin-stimulated lipolysis in WAT. 5. FGF21-inhibited lipolysis was mediated by Akt-dependent reduction of cyclic adenosine monophosphate (cAMP) levels in both mouse and human WAT. 6. FGF21 KO mice were resistant to diet- and aging-induced obesity, which was attributed to decreased fat mass. The increased lipolysis and fatty acid oxidation in FGF21 KO mice may explain in part the lean phenotype of FGF21 KO mice. Conclusions: These results collectively suggest FGF21 as a key modulator of glucose and lipid metabolism in WAT, by activation of ERK1/2 kinase and Akt respectively. FGF21 and its signaling components may represent potential targets for the future development of new strategies for treating obesity and its medical complications.
published_or_final_version
Medicine
Doctoral
Doctor of Philosophy

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Christensen, Randolph N. "Fibroblast growth factors and the Apical Epithelial Cap in Axolotl (Ambystoma mexicanum) limb regeneration /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486399160104861.

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