华西虚拟期刊

华西虚拟期刊

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Kruppel-like Factor 4 (KLF4), a target gene of miR-145, can negatively regulate lung fibrosis. However, the potential role of KLF4 and miR-145 in hepatic stellate cells (HSCs) activation or in hepatic fibrosis keeps unclear. This study aims to characterize miR-145 and KLF4 in activated HSCs and liver cirrhotic, and the underlying molecular basis. miR-145 was significantly up-regulated, while KLF4 was dramatically down-regulated during the activation of rat primary HSCs and TGF-beta treated HSCs. Furthermore, miR-145 mimics induced and inhibition of miR-145 reduced a-SMA and COL-I expression in primary HSCs. Additionally, the mRNA and protein levels of KLF4 in the liver of cirrhotic patients and rats were significantly down-regulated. alpha-SMA and COL-I were increased after inhibition of KLF4 by specific shRNA in primary HSCs. Forced KLF4 expression led to a reduction of a-SMA and COL-I expression in HSCs. miR-145 promotes HSC activation and liver fibrosis by targeting KLF4.

Key words: GROWTH-FACTOR-BETA; LIVER FIBROSIS; GASTRIC-CANCER; MIR-145; DIFFERENTIATION; PROLIFERATION; EXPRESSION; KLF4; MICRORNAS; REGULATOR

引用本文: . . 华西虚拟期刊, 2000, 1(1): -. doi: 10.1038/srep40468 复制

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