The role of the miR-31/FIH1 pathway in TGF-β-induced liver fibrosis

• DOI: 10.1042/cs20140012
• Publication Date: 2015-03-03T16:54:29Z
• Authors: Jiangfeng Hu; Chao Chen; Qidong Liu; Baohai Liu; Chenlin Song; Songchen Zhu; Chaoqun Wu; Su Liu; Hongyu Yu; Dingkang Yao; Jiuhong Kang; Liang Zhu
• Keywords: Hepatic stellate cell; Hepatic fibrosis

The miRNAs are small, non-coding RNAs that regulate various biological processes, including liver fibrosis. Hepatic stellate cells (HSCs) play a central role in the pathogenesis of By microarray profiling and real-time PCR, we noted miR-31 expression HSCs from rats, mice humans was significantly increased during HSC activation culture. Overall, levels were unchanged whole-liver RNA extracts fibrotic rat human samples. Nevertheless, found particularly up-regulated but not hepatocytes fibrogenesis. Thus, hypothesized may mediate In present study, inhibition inhibited activation, whereas its over-expression obviously promoted activation. Moreover, migration by enhancing matrix metalloproteinase (MMP)-2 has an opposite effect. function might be through targeting FIH1, suppressor hypoxia-inducible factor (HIF-1), because knockdown FIH1 shRNA could mimic effects miR-31. addition, primary isolated treated with different cytokines, such as transforming growth β (TGF-β), vascular endothelial platelet-derived factor-BB, to evaluate upstream regulators We only TGF-β, pivotal regulator fibrosis, remarkably HSCs. And TGF-β on can partially counteracted chromatin immunoprecipitation experiments luciferase reporter assay demonstrated Smad3, major TGF-β-downstream transcription factor, stimulated activity binding directly miR-31's promoter. conclusion, miR-31/FIH1 pathway associates perhaps participation TGF-β/Smad3 signalling