TAILIEUCHUNG - Báo cáo khoa học: FGF-2, IL-1b and TGF-b regulate fibroblast expression of S100A8

Growth factors, including fibroblast growth factor-2 (FGF-2) and transform-ing growth factor-b(TGF-b) regulate fibroblast function, differentiation and proliferation. S100A8 and S100A9 are members of the S100 family of Ca 2+ -binding proteins and are now accepted as markers of inflammation. They are expressed by keratinocytes and inflammatory cells in human⁄murine wounds and by appropriately activated macrophages, endothelial cells, epithelial cells and keratinocytesin vitro. | ềFEBS Journal FGF-2 IL-1 b and TGF-p regulate fibroblast expression of S100A8 Farid Rahimi Kenneth Hsu Yasumi Endoh and Carolyn L. Geczy Inflammatory Diseases Research Unit Schoolof MedicalSciences University of New South Wales Sydney Australia Keywords FGF-2 fibroblasts interleukin-1 b S100A8 gene TGF-b Correspondence C. Geczy Inflammatory Diseases Research Unit Schoolof MedicalSciences The University of New South Wales Sydney NSW 2052 Australia Fax 61 293851389 Tel 61 293851599 E-mail Website http Received 3 March 2005 revised 28 March 2005 accepted 5 April 2005 doi Growth factors including fibroblast growth factor-2 FGF-2 and transforming growth factor-b TGF-b regulate fibroblast function differentiation and proliferation. S100A8 and S100A9 are members of the S100 family of Ca2 -binding proteins and are now accepted as markers of inflammation. They are expressed by keratinocytes and inflammatory cells in human murine wounds and by appropriately activated macrophages endothelial cells epithelial cells and keratinocytes in vitro. In this study regulation and expression of S100A8 and S100A9 were examined in fibroblasts. Endotoxin LPS interferon c IFNc tumour-necrosis factor TNF and TGF-b did not induce the S100A8 gene in murine fibroblasts whereas FGF-2 induced mRNA maximally after 12 h. The FGF-2 response was strongly enhanced and prolonged by heparin. Interleukin-1 b IL-1b alone or in synergy with FGF-2 heparin strongly induced the gene in 3T3 fibroblasts. S100A9 mRNA was not induced under any condition. Induction of S100A8 in the absence of S100A9 was confirmed in primary fibroblasts. S100A8 mRNA induction by FGF-2 and IL-1b was partially dependent on the mitogen-activated-protein-kinase pathway and dependent on new protein synthesis. FGF-2-responsive elements were distinct from the IL-1b-responsive elements in the S100A8 gene promoter. FGF-2- heparin-induced but not IL-1b-induced responses

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