Gefitinib attenuates transforming growth factor-β1–activated mitogen-activated protein kinases and mitogenesis in NRK-49F cells
作者： San-Cher Chen , Jinn-Yuh Guh , Tai-Du Lin , Shean-Jaw Chiou , Chi-Ching Hwang
DOI: 10.1016/J.TRSL.2011.06.002
关键词:
摘要: Transforming growth factor-β (TGF-β), TGF-β receptor (TGF-βR), and epidermal factor (EGFR) are important in the pathogenesis of kidney fibrosis, a result renal fibroblast activation. The EGFR kinase inhibitor gefitinib attenuates glomerular fibrosis hypertensive rats whereas dominant-negative interstitial mouse with acute ischemia. Thus, we studied effects molecular mechanisms TGF-β1–induced mitogenesis collagen production normal rat (NRK-49F) cells. We found that TGF-β1 increased cell mitogenesis. also time-dependently cyclin D1 protein expression. rapidly transactivated EGFR. SB431542 (a type I TGF-βR inhibitor) SB203580 p38 attenuated phosphorylation Smad2/3 protein. ERK1/2 kinase. Moreover, SB431542, gefitinib, PD98059 (an inhibitor), Finally, production. concluded via EGFR-ERK1/2/p38 pathway NRK-49F expression in vitro .
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