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FGF2 — HGF

Text-mined interactions from Literome

Blanquaert et al., Endocrinology 1999 : Fibroblast growth factor-2 induces hepatocyte growth factor/scatter factor expression in osteoblasts ... We investigated the effect of fibroblast growth factor-2 (FGF-2) on the expression of HGF/SF and its receptor, encoded by c-met, in the MC3T3-E1 osteoblastic cell line ... FGF-2 also induced HGF/SF polypeptide synthesis ... The stimulation of HGF/SF mRNA expression by FGF-2 was blocked by cycloheximide, a protein synthesis inhibitor, but not by DNA or prostaglandin synthesis inhibitors ... FGF-2 increased the rate of HGF/SF gene transcription by approximately 2-fold, as determined by nuclear run-on assays, and did not modify the decay of HGF/SF mRNA in transcriptionally arrested cells ... In conclusion, FGF-2 induces HGF/SF expression in osteoblasts and may promote HGF/SF activity by increasing the expression of its receptor
Hashimoto et al., Development 1999 : HOXA-11 expression in both myogenic precursor cells and mesenchyme was induced by fibroblast growth factor ( FGF ) signal, whereas hepatocyte growth factor/scatter factor ( HGF/SF ) maintained HOXA-11 expression in the myogenic precursor cells, but not in the mesenchyme
Yoshida et al., J Clin Endocrinol Metab 2002 (Endometrial Neoplasms...) : Induction of hepatocyte growth factor in stromal cells by tumor derived basic fibroblast growth factor enhances growth and invasion of endometrial cancer ... Basic fibroblast growth factor derived from tumor cells may induce HGF in endometrial stromal cells, whereas stromal cell derived HGF leads to the invasive growth of carcinoma cells
Onimaru et al., Circ Res 2002 (Disease Models, Animal...) : Fibroblast growth factor-2 gene transfer can stimulate hepatocyte growth factor expression irrespective of hypoxia mediated downregulation in ischemic limbs ... Mice deficient in basic fibroblast growth factor-2 ( FGF-2 ) showed reduced induction of HGF protein in ischemic muscles, and overexpression of FGF-2 via gene transfer stimulated endogenous HGF, irrespective of the presence of ischemia ... FGF-2 mediated induction of HGF was fully dependent on the mitogen activated protein kinase pathway yet was not affected by either hypoxia or a protein kinase A inhibitor
Hollborn et al., Graefes Arch Clin Exp Ophthalmol 2004 : Beside the stimulation of cell proliferation, which is dependent on activation of p44/p42 and p38 MAPKs, bFGF induces the secretion of VEGF and HGF by Müller cells
Naim et al., In Vivo 2005 (Cholesteatoma, Middle Ear...) : We assume that HGF/SF released FGF-2 in the matrix but did not induce FGF-2 expression
Eto et al., Lab Invest 2012 (Cicatrix, Hypertrophic) : Decreased MMP-1 expression may be an important transcriptional change in HTS, and its reversal as well as upregulation of HGF by FGF-2 could be a new therapeutic approach for HTS
Kaga et al., Vascul Pharmacol 2012 (Inflammation) : In addition, bFGF , but not HGF or VEGF, significantly activated an essential transcription factor for inflammation, NF?B, and gene expression of its downstream inflammation related cytokines ( IL-8 and MCP-1 ) in VSMCs, accompanied by an increase in the vascular permeability in the rat paper disc model
Chang et al., J Cell Mol Med 2012 : It was found that basic fibroblast growth factor , epidermal growth factor and ascorbic acid 2-phosphate promoted HGF secretion in MSCs
Stachon et al., Graefes Arch Clin Exp Ophthalmol 2013 : Photodynamic inactivation triggers FGFb and inhibits HGF secretion of keratocytes transiently ( 5 hours ) and inhibits KGF secretion 24 hours following treatment
Roletto et al., J Cell Physiol 1996 : Basic fibroblast growth factor stimulates hepatocyte growth factor/scatter factor secretion by human mesenchymal cells
Heymann et al., Dev Biol 1996 : This demonstrates that the initial induction of SF/HGF by FGF does not require limb formation
Gulati et al., Endocrinology 1997 : This concept is based on the observations that : 1 ) in the presence of the calcium chelator BAPTA, HGF/SF decreased cell contact but did not increase [ Ca2+ ] i or apoptosis ; 2 ) bFGF blocked HGF/SF induced increase in [ Ca2+ ] i ; 3 ) bFGF did not attenuate HGF/SF 's apoptotic action if exposed to cells after the increase in [ Ca2+ ] i ; and 4 ) RNA and protein synthesis were required for HGF/SF to increase [ Ca2+ ] i, whereas the thapsigargin- and Bay K-induced increase in [ Ca2+ ] i and apoptosis were independent of RNA/protein synthesis
Kumar et al., Int J Oncol 1998 : HGF, bFGF , and VEGF/VPF induced chemotactic migration of the endothelial cells, but only HGF ( scatter factor ) enhanced nondirectional motility