TGF-β1Regulate Of Kruppel-like Factor15(KLF15) And Its Mechanism

Objective: Discuss the impact of TGF-β1on Kruppel-like Factor15(KLF15)expression and the regulatory mechanismMethods: Culturing rat normal kidney fibroblast cells (NRK-49F), gived TGF-β1stimulation and overpressed KLF15by transient transfection. We observed extracellularmatrix（ECM）change through the Real-time PCR detection KLF15mRNA and FNmRNA,CTGFmRNA, COL Ⅲ mRNA. To observe change of the amount of KLF15and CTGFprotein expression by Western blot means. By the ELSA method detect the cell culturesupernatant FN protein and collagen type Ⅲ changes. Prior to stimulation of NRK-49Fwith TGF-β1, cells were pretreated with the mitogen-activated protein kinase (MAPK)cell signaling pathway-specific blocking agent. We observa the FNmRNA, CTGFmRNA,COL Ⅲ mRNA,KLF15mRNA changes by Real-time PCR and KLF15, CTGF proteinand related protein phosphorylation changed by Western Blot.Results: TGF-β1stimulation the rat normal kidney fibroblast cells (NRK-49F) canpromote the secretion of extracellular matrix and inhibit the expression of KLF15.Extracellular matrix expression was significantly downregulated after overexpression ofKLF15. ERK/MAPK and JNK/MAPK pathway blockers attenuated the inhibitory effect ofTGF-β1on KLF15but given P38/MAPK pathway blockers did not inhibit the effect ofTGF-β1downregulated KLF15.Conclusion: KLF15inhibit extracellular matrix production. TGF-β1may throughERK/MAPK and JNK/MAPK signal pathway inhibit KLF15expression to promote thegeneration of extracellular matrix.