Regulation of connective tissue growth factor gene expression in human skin fibroblasts and during wound repair.
作者： A Igarashi , H Okochi , D M Bradham , G R Grotendorst
DOI: 10.1091/MBC.4.6.637
关键词: Growth factor receptor inhibitor 、 Cell biology 、 Growth factor 、 Biology 、 Basic fibroblast growth factor 、 CTGF 、 Molecular biology 、 Transforming growth factor beta 、 Platelet-derived growth factor 、 Epidermal growth factor 、 Platelet-derived growth factor receptor
摘要: Connective tissue growth factor (CTGF) is a cysteine-rich peptide that exhibits platelet-derived (PDGF)-like biological and immunological activities. CTGF member of family peptides include serum-induced immediate early gene products, v-src-induced peptide, putative avian transforming gene, nov. In the present study, we demonstrate human foreskin fibroblasts produce high levels mRNA protein after activation with beta (TGF-beta) but not other factors including PDGF, epidermal factor, basic fibroblast factor. Because level selective induction by TGF-beta, it appears major autocrine produced TGF-beta-treated skin fibroblasts. Cycloheximide did block large TGF-beta stimulation expression, indicating directly regulated TGF-beta. Similar regulatory mechanisms appear to function in vivo during wound repair where there coordinate expression 1 before regenerating tissue, suggesting cascade process for control regeneration repair.
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