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Relevant bibliographies by topics / Fibroblast growth factors

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Academic literature on the topic 'Fibroblast growth factors'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2024

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Journal articles on the topic "Fibroblast growth factors"

1

Thomas, Kenneth A. "Fibroblast growth factors." FASEB Journal 1, no. 6 (December 1987): 434–40. http://dx.doi.org/10.1096/fasebj.1.6.3315806.

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Baird, Andrew, and Patricia A. Walicke. "Fibroblast growth factors." British Medical Bulletin 45, no. 2 (1989): 438–52. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072333.

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Mason, Ivor. "Fibroblast growth factors." Current Biology 13, no. 9 (April 2003): R346. http://dx.doi.org/10.1016/s0960-9822(03)00270-7.

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Cheng, Maye F., Faizah S. Abdullah, and Matthew B. Buechler. "Essential growth factor receptors for fibroblast homeostasis and activation: Fibroblast Growth Factor Receptor (FGFR), Platelet Derived Growth Factor Receptor (PDGFR), and Transforming Growth Factor β Receptor (TGFβR)." F1000Research 13 (May 21, 2024): 120. http://dx.doi.org/10.12688/f1000research.143514.2.

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Fibroblasts are cells of mesenchymal origin that are found throughout the body. While these cells have several functions, their integral roles include maintaining tissue architecture through the production of key extracellular matrix components, and participation in wound healing after injury. Fibroblasts are also key mediators in disease progression during fibrosis, cancer, and other inflammatory diseases. Under these perturbed states, fibroblasts can activate into inflammatory fibroblasts or contractile myofibroblasts. Fibroblasts require various growth factors and mitogenic molecules for survival, proliferation, and differentiation. While the activity of mitogenic growth factors on fibroblasts in vitro was characterized as early as the 1970s, the proliferation and differentiation effects of growth factors on these cells in vivo are unclear. Recent work exploring the heterogeneity of fibroblasts raises questions as to whether all fibroblast cell states exhibit the same growth factor requirements. Here, we will examine and review existing studies on the influence of fibroblast growth factor receptors (FGFRs), platelet-derived growth factor receptors (PDGFRs), and transforming growth factor β receptor (TGFβR) on fibroblast cell states.

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Cheng, Maye F., Faizah S. Abdullah, and Matthew B. Buechler. "Essential growth factor receptors for fibroblast homeostasis and activation." F1000Research 13 (February 19, 2024): 120. http://dx.doi.org/10.12688/f1000research.143514.1.

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Fibroblasts are cells of mesenchymal origin that are found throughout the body. While these cells have several functions, their integral roles include maintaining tissue architecture through the production of key extracellular matrix components, and participation in wound healing after injury. Fibroblasts are also key mediators in disease progression during fibrosis, cancer, and other inflammatory diseases. Under these perturbed states, fibroblasts can activate into inflammatory fibroblasts or contractile myofibroblasts. Fibroblasts require various growth factors and mitogenic molecules for survival, proliferation, and differentiation. While the activity of mitogenic growth factors on fibroblasts in vitro was characterized as early as the 1970s, the proliferation and differentiation effects of growth factors on these cells in vivo are unclear. Moreover, recent work exploring the heterogeneity of fibroblasts raises questions as to whether all fibroblast cell states exhibit the same growth factor requirements. Here, we will examine and review existing growth factors known to influence fibroblast homeostasis to begin unpacking the potential growth factors that may influence in vivo fibroblast cell states.

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Chen, Gregory, and Reza Forough. "Fibroblast Growth Factors, Fibroblast Growth Factor Receptors, Diseases, and Drugs." Recent Patents on Cardiovascular Drug Discovery 1, no. 2 (June 1, 2006): 211–24. http://dx.doi.org/10.2174/157489006777442478.

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Onoue, H., Y. Ebi, H. Nakayama, XM Ru, Y. Kitamura, and J. Fujita. "Suppressive effect of Sl/Sld mouse embryo-derived fibroblast cell lines on diffusible factor-dependent proliferation of mast cells." Blood 74, no. 5 (October 1, 1989): 1557–62. http://dx.doi.org/10.1182/blood.v74.5.1557.1557.

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Abstract Two modes of mast cell growth are present, one dependent on diffusible growth factors (interleukins [IL] 3 and 4) and another dependent on contact with fibroblasts. The 3T3 fibroblast cell lines derived from WCB6F1-+/+ mouse embryos supported the proliferation of cultured mast cells (CMC), whereas the 3T3 fibroblast cell lines from WCB6F1-Sl/Sld mouse embryos did not. To investigate the relationship between growth factor-dependent and fibroblast-dependent growths of mast cells, we cocultured CMC and 3T3 fibroblasts in the presence of diffusible growth factors. WCB6F1-+/+ mouse embryo-derived 3T3 cells did not affect the growth factor-dependent proliferation of CMC, but WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells significantly suppressed the proliferation. Close cell-to-cell contact was necessary for the suppression. The NWS1 fibroblast cell line was established from the spleen cells of an adult WBB6F1-+/+ mouse. Although the NWS1 cell line had no supporting effect on the proliferation of CMC in the absence of diffusible growth factors, it did not suppress the proliferation of CMC induced by the growth factors. The present result suggests that a product of mutant Sl genes may be involved in the suppressive activity of WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells.

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Onoue, H., Y. Ebi, H. Nakayama, XM Ru, Y. Kitamura, and J. Fujita. "Suppressive effect of Sl/Sld mouse embryo-derived fibroblast cell lines on diffusible factor-dependent proliferation of mast cells." Blood 74, no. 5 (October 1, 1989): 1557–62. http://dx.doi.org/10.1182/blood.v74.5.1557.bloodjournal7451557.

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Two modes of mast cell growth are present, one dependent on diffusible growth factors (interleukins [IL] 3 and 4) and another dependent on contact with fibroblasts. The 3T3 fibroblast cell lines derived from WCB6F1-+/+ mouse embryos supported the proliferation of cultured mast cells (CMC), whereas the 3T3 fibroblast cell lines from WCB6F1-Sl/Sld mouse embryos did not. To investigate the relationship between growth factor-dependent and fibroblast-dependent growths of mast cells, we cocultured CMC and 3T3 fibroblasts in the presence of diffusible growth factors. WCB6F1-+/+ mouse embryo-derived 3T3 cells did not affect the growth factor-dependent proliferation of CMC, but WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells significantly suppressed the proliferation. Close cell-to-cell contact was necessary for the suppression. The NWS1 fibroblast cell line was established from the spleen cells of an adult WBB6F1-+/+ mouse. Although the NWS1 cell line had no supporting effect on the proliferation of CMC in the absence of diffusible growth factors, it did not suppress the proliferation of CMC induced by the growth factors. The present result suggests that a product of mutant Sl genes may be involved in the suppressive activity of WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells.

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Metzler, Veronika Maria, Christian Pritz, Anna Riml, Angela Romani, Raphaela Tuertscher, Teresa Steinbichler, Daniel Dejaco, Herbert Riechelmann, and József Dudás. "Separation of cell survival, growth, migration, and mesenchymal transdifferentiation effects of fibroblast secretome on tumor cells of head and neck squamous cell carcinoma." Tumor Biology 39, no. 11 (November 2017): 101042831770550. http://dx.doi.org/10.1177/1010428317705507.

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Fibroblasts play a central role in tumor invasion, recurrence, and metastasis in head and neck squamous cell carcinoma. The aim of this study was to investigate the influence of tumor cell self-produced factors and paracrine fibroblast–secreted factors in comparison to indirect co-culture on cancer cell survival, growth, migration, and epithelial–mesenchymal transition using the cell lines SCC-25 and human gingival fibroblasts. Thereby, we particularly focused on the participation of the fibroblast-secreted transforming growth factor beta-1.Tumor cell self-produced factors were sufficient to ensure tumor cell survival and basic cell growth, but fibroblast-secreted paracrine factors significantly increased cell proliferation, migration, and epithelial–mesenchymal transition–related phenotype changes in tumor cells. Transforming growth factor beta-1 generated individually migrating disseminating tumor cell groups or single cells separated from the tumor cell nest, which were characterized by reduced E-cadherin expression. At the same time, transforming growth factor beta-1 inhibited tumor cell proliferation under serum-starved conditions. Neutralizing transforming growth factor beta antibody reduced the cell migration support of fibroblast-conditioned medium. Transforming growth factor beta-1 as a single factor was sufficient for generation of disseminating tumor cells from epithelial tumor cell nests, while other fibroblast paracrine factors supported tumor nest outgrowth. Different fibroblast-released factors might support tumor cell proliferation and invasion, as two separate effects.

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COUTTS, JACQUELINE C., and JOHN T. GALLAGHER. "Receptors for fibroblast growth factors." Immunology and Cell Biology 73, no. 6 (December 1995): 584–89. http://dx.doi.org/10.1038/icb.1995.92.

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Dissertations / Theses on the topic "Fibroblast growth factors"

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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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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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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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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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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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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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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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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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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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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Books on the topic "Fibroblast growth factors"

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Baird, Andrew, 1954 July 27-, Klagsbrun Michael, and New York Academy of Sciences., eds. The Fibroblast growth factor family. New York, N.Y: New York Academy of Sciences, 1991.

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2

Pedro, Cuevas, ed. Fibroblast growth factor in the cardiovascular system. Munich: I. Holzapfel, 2002.

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Mullen, Elizabeth Anne. An inhibitor of angiogenesis isolated from bovine cornea. [s.l: s.n.], 1992.

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Drucker, Beverly Joyce. Functional and developmental studies on members of the fibroblast growth factor family. [New York]: [Columbia University], 1993.

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Dalton, Stephen Lewis. Cell attachment controls fibronectin and α51 integrin levels in fibroblasts: Implications for anchorage-dependent and -independent growth. [New York]: [Columbia University], 1993.

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Westman, Jacob. Synthesis of oligosaccharides related to heparin and heparan sulphate and their binding to fibroblast growth factors. Stockholm, Sweden: Dept. of Organic Chemistry, Arrhenius Laboratory, Stockholm University, 1995.

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1945-, Lippman Marc E., Ortho Pharmaceutical Corporation, and University of California, Los Angeles., eds. Growth regulation of cancer: Proceedings of an Ortho-UCLA Symposium on Growth Regulation of Cancer, held at Park City, Utah, January 17-23, 1987. New York: Liss, 1988.

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Kjell, Fuxe, and Wenner-Grenska samfundet, eds. Trophic regulation of the basal ganglia: Focus on dopamine neurons. Oxford, OX, UK: Pergamon, 1994.

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1945-, Lippman Marc E., Dickson Robert B. 1952-, and University of California, Los Angeles., eds. Growth regulation of cancer II: Proceedings of a UCLA symposium, held at Keystone, Colorado, January 21-27, 1989. New York: Wiley-Liss, 1990.

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Walters, Jean Elizabeth. Immunochemical studies on fibroblast growth factor-1 and fibroblast growth factor receptor 1. Oxford: Oxford Brookes University, 1998.

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Book chapters on the topic "Fibroblast growth factors"

1

Baird, A., and P. Böhlen. "Fibroblast Growth Factors." In Peptide Growth Factors and Their Receptors I, 369–418. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-49295-2_7.

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Cronauer, Marcus V., and Wolfgang A. Schulz. "Fibroblast Growth Factors." In Encyclopedia of Cancer, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2175-2.

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Baird, A., and P. Böhlen. "Fibroblast Growth Factors." In Peptide Growth Factors and Their Receptors I, 369–418. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3210-0_7.

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Cronauer, Marcus V., and Wolfgang A. Schulz. "Fibroblast Growth Factors." In Encyclopedia of Cancer, 1717–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_2175.

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Cronauer, Marcus V., and Wolfgang A. Schulz. "Fibroblast Growth Factors." In Encyclopedia of Cancer, 1397–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2175.

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Chiodelli, Paola, and Marco Presta. "Fibroblast Growth Factors." In Encyclopedia of Molecular Pharmacology, 1–11. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_5710-1.

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Chiodelli, Paola, and Marco Presta. "Fibroblast Growth Factors." In Encyclopedia of Molecular Pharmacology, 665–75. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_5710.

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Moscatelli, David. "Fibroblast Growth Factors." In Cytokines of the Lung, 41–76. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003066927-3.

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Ornitz, David M., and Gabriel Waksman. "Fibroblast Growth Factor Receptors." In Growth Factors and Wound Healing, 151–74. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-1876-0_9.

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Burgess, Wilson H. "Structure-Function Analysis of Fibroblast Growth Factor-1 (Acidic Fibroblast Growth Factor)." In Growth Factors, Peptides and Receptors, 297–308. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2846-3_28.

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Conference papers on the topic "Fibroblast growth factors"

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Hurley, Jennifer R., and Daria A. Narmoneva. "Fibroblasts Induce Mechanical Changes in the Extracellular Environment and Enhance Capillary-Like Network Formation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193093.

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Cardiac tissue engineering studies have demonstrated the importance of revascularization in engineered grafts for successful implantation and regeneration [1]. Understanding the myocardium’s complex cellular organization and the interactions between the major cardiac cell types (cardiomyocytes, endothelial cells, and cardiac fibroblasts) is critical for revascularization. Our previous studies have shown the importance of cardiomyocyte-endothelial interactions [2]. However, there is limited information available on endothelial-fibroblast interactions. We and others have previously observed that during capillary assembly, fibroblasts provide chemical signaling via expression of growth factors [3, 4]. In addition, fibroblasts may also regulate angiogenesis through alterations to the mechanical environment via myocardial remodeling, including matrix degradation and deposition, and tissue contraction. Changes to the extracellular mechanical enviroment may lead to changes in basic cell functions such as proliferation, apoptosis, and growth factor expression.

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Kwon, Youngjoo, and Geun Yeong Park. "Abstract 5088: Fibroblast-derived factors enhance growth of ovarian cancer cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5088.

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Seitz, T., K. Freese, WE Thasler, and C. Hellerbrand. "Expression of paracrine fibroblast growth factors in hepatic stellate cells and hepatic fibrosis." In 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1721957.

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Woo, K. V., C. Weinheimer, J. Nigro, and D. M. Ornitz. "Protective Role of Fibroblast Growth Factors in Group 3 Hypoxia Induced Pulmonary Hypertension." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4033.

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Singh, Ankur, Shalu Suri, Ted T. Lee, Jamie M. Chilton, Steve L. Stice, Hang Lu, Todd C. McDevitt, and Andrés J. Garcia. "Adhesive Signature-Based, Label-Free Isolation of Human Pluripotent Stem Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80044.

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Generation of human induced pluripotent stem cells (hiPSCs) from fibroblasts and other somatic cells represents a highly promising strategy to produce auto- and allo-genic cell sources for therapeutic approaches as well as novel models of human development and disease1. Reprogramming protocols involve transduction of the Yamanaka factors Oct3/4, Sox2, Klf4, and c-Myc into the parental somatic cells, followed by culturing the transduced cells on mouse embryonic fibroblast (MEF) or human fibroblast feeder layers, and subsequent mechanical dissociation of pluripotent cell-like colonies for propagation on feeder layers1, 2. The presence of residual parental and feeder-layer cells introduces experimental variability, pathogenic contamination, and promotes immunogenicity3. Similar to human embryonic stem cells (hESCs), reprogrammed hiPSCs suffer from the unavoidable problem of spontaneous differentiation due to sub-optimal feeder cultures4, growth factors5, and the feeder-free substrate6. Spontaneously differentiated (SD)-hiPSCs display reduced pluripotency and often contaminate hiPSC cultures, resulting in overgrowth of cultures and compromising the quality of residual pluripotent stem cells5. Therefore, the ability to rapidly and efficiently isolate undifferentiated hiPSCs from the parental somatic cells, feeder-layer cells, and spontaneously differentiated cells is a crucial step that remains a bottleneck in all human pluripotent stem cell research.

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Rieke, Damian T., Zhixiang Zuo, Katharina Endhardt, Michaela Keck, Arun Khattri, Derya Mahmutoglu, Kelley Leung, Mohamed El Dinali, Johannes Braegelmann, and Tanguy Y. Seiwert. "Abstract 2832: Fibroblast growth factors in head and neck cancer: Genetic alterations and therapeutic targeting with ponatinib." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2832.

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Epstein Shochet, Gali, Becky Bardenstein-Wald, Elizabetha Brook, and David Shitrit. "Transforming growth factor beta (TGF-ß) pathway activation by IPF fibroblast-derived soluble factors is mediated by IL-6 trans-signaling." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3352.

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Guzy, R., B. Ansbro, E. Reed, and N. O. Dulin. "Fibroblast Growth Factor 2 Accelerates Myofibroblast Dedifferentiation in Primary Human Lung Fibroblasts." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4042.

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Shreiber, David I., Paul A. J. Enever, and Robert T. Tranquillo. "Stress-Dependent Effects of Platelet-Derived Growth Factor-BB on Fibroblast Migration and Traction Differ in Collagen and Fibrin." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2575.

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Abstract We used our novel assays of cell behavior in tissue equivalents to study the dose-response effects of PDGF-BB on RDF migration and traction in mechanically stressed and stress-free type I collagen and fibrin gels. PDGF-BB increased fibroblast migration significantly in all assays, but the effects on traction depended on the presence of stress and the nature of the ECM. PDGF-BB decreased fibroblast traction in stressed collagen gels, but increased traction in stress-free gels. No statistical conclusion could be inferred for stressed fibrin gels, and increasing PDGF-BB decreased traction in stress-free fibrin gels. These results demonstrate the complex response of fibroblasts to environmental cues, and point to opportunities to orchestrate cell behavior to affect the outcome of wound healing.

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Gould, Russell, Karen Chin, Puifai Santisakultam, Amanda Dropkin, Jennifer Richards, Yung-Nung Chiu, Chris Schaffer, and Jonathan Butcher. "Anisotropic Strain Fields Enhance Matrix Remodeling Through Elevated TGF-β Signaling." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53805.

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In this work, we demonstrate the unique effect of controlled anisotropic strain on fibroblast behavior in 3D engineered tissue environments. Anisotropy of biaxial strain resulted in increased cellular orientation and collagen fiber alignment. Transforming growth factor beta-1 (TGFβ1) gene expression and pSmad2 nuclear translocation increased with biaxial directionality. Myofibroblastic alpha-smooth muscle actin (α-SMA) decreased with applied strain similar to mechanically unloaded hydrogels. Collectively, these results demonstrate a novel mechanobiological mechanism by which fibroblasts develop rapid anisotropic matrix striation while maintaining phenotype quiescence.

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Reports on the topic "Fibroblast growth factors"

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Funkenstein, Bruria, and Shaojun (Jim) Du. Interactions Between the GH-IGF axis and Myostatin in Regulating Muscle Growth in Sparus aurata. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7696530.bard.

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Growth rate of cultured fish from hatching to commercial size is a major factor in the success of aquaculture. The normal stimulus for muscle growth in growing fish is not well understood and understanding the regulation of muscle growth in fish is of particular importance for aquaculture. Fish meat constitutes mostly of skeletal muscles and provides high value proteins in most people's diet. Unlike mammals, fish continue to grow throughout their lives, although the size fish attain, as adults, is species specific. Evidence indicates that muscle growth is regulated positively and negatively by a variety of growth and transcription factors that control both muscle cell proliferation and differentiation. In particular, growth hormone (GH), fibroblast growth factors (FGFs), insulin-like growth factors (IGFs) and transforming growth factor-13 (TGF-13) play critical roles in myogenesis during animal growth. An important advance in our understanding of muscle growth was provided by the recent discovery of the crucial functions of myostatin (MSTN) in controlling muscle growth. MSTN is a member of the TGF-13 superfamily and functions as a negative regulator of skeletal muscle growth in mammals. Studies in mammals also provided evidence for possible interactions between GH, IGFs, MSTN and the musclespecific transcription factor My oD with regards to muscle development and growth. The goal of our project was to try to clarify the role of MSTNs in Sparus aurata muscle growth and in particular determine the possible interaction between the GH-IGFaxis and MSTN in regulating muscle growth in fish. The steps to achieve this goal included: i) Determining possible relationship between changes in the expression of growth-related genes, MSTN and MyoD in muscle from slow and fast growing sea bream progeny of full-sib families and that of growth rate; ii) Testing the possible effect of over-expressing GH, IGF-I and IGF-Il on the expression of MSTN and MyoD in skeletal muscle both in vivo and in vitro; iii) Studying the regulation of the two S. aurata MSTN promoters and investigating the possible role of MyoD in this regulation. The major findings of our research can be summarized as follows: 1) Two MSTN promoters (saMSTN-1 and saMSTN-2) were isolated and characterized from S. aurata and were found to direct reporter gene activity in A204 cells. Studies were initiated to decipher the regulation of fish MSTN expression in vitro using the cloned promoters; 2) The gene coding for saMSTN-2 was cloned. Both the promoter and the first intron were found to be polymorphic. The first intron zygosity appears to be associated with growth rate; 3) Full length cDNA coding for S. aurata growth differentiation factor-l I (GDF-II), a closely related growth factor to MSTN, was cloned from S. aurata brain, and the mature peptide (C-terminal) was found to be highly conserved throughout evolution. GDF-II transcript was detected by RT -PCR analysis throughout development in S. aurata embryos and larvae, suggesting that this mRNA is the product of the embryonic genome. Transcripts for GDF-Il were detected by RT-PCR in brain, eye and spleen with highest level found in brain; 4) A novel member of the TGF-Bsuperfamily was partially cloned from S. aurata. It is highly homologous to an unidentified protein (TGF-B-like) from Tetraodon nigroviridisand is expressed in various tissues, including muscle; 5) Recombinant S. aurata GH was produced in bacteria, refolded and purified and was used in in vitro and in vivo experiments. Generally, the results of gene expression in response to GH administration in vivo depended on the nutritional state (starvation or feeding) and the time at which the fish were sacrificed after GH administration. In vitro, recombinantsaGH activated signal transduction in two fish cell lines: RTHI49 and SAFI; 6) A fibroblastic-like cell line from S. aurata (SAF-I) was characterized for its gene expression and was found to be a suitable experimental system for studies on GH-IGF and MSTN interactions; 7) The gene of the muscle-specific transcription factor Myogenin was cloned from S. aurata, its expression and promoter activity were characterized; 8) Three genes important to myofibrillogenesis were cloned from zebrafish: SmyDl, Hsp90al and skNAC. Our data suggests the existence of an interaction between the GH-IGFaxis and MSTN. This project yielded a great number of experimental tools, both DNA constructs and in vitro systems that will enable further studies on the regulation of MSTN expression and on the interactions between members of the GHIGFaxis and MSTN in regulating muscle growth in S. aurata.

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Welling, Bradley. Fibroblast Growth Factor Regeneration of Tympanic Membrane Perforations. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada591173.

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Ittmann, Michael M. Fibroblast Growth Factor Receptor-4 and Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada446482.

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Ittmann, Michael M. Fibroblast Growth Factor Receptor-4 and Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada462818.

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Ittmann, Michael M. Fibroblast Growth Factor Receptor-4 and Prostate Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada476956.

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Kagan, Benjamin L. Growth Factor Regulation of an Angiogenic Factor, the Fibroblast Growth Factor-Binding Protein (FGF-BP), in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada398106.

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Kagan, Benjamin L. Growth Factor Regulation of an Angiogenic Factor, the Fibroblast Growth Factor-Binding Protein (FGF-BP), in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada410065.

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Wieder, Robert. The Role of Basic Fibroblast Growth Factor in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada302241.

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Tondravi, Mehrdad. Optimization of Fibroblast Growth Factor-1 as an Anabolic Agent for Osteoporosis. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada394773.

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Burgess, Wilson H. Optimization of Fibroblast Growth Factor-1 as an Anabolic Agent for Osteoporosis. Fort Belvoir, VA: Defense Technical Information Center, October 1997. http://dx.doi.org/10.21236/adb233740.

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