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Background  MicroRNA-21 (miR-21) plays an important role in the pathogenesis and progression of liver fibrosis. Here, we determined the serum and hepatic content of miR-21 in patients with liver cirrhosis and rats with dimethylnitrosamine-induced hepatic cirrhosis and examined the effects of miR-21 on  SPRY2  and  HNF4α  in modulating ERK1 signaling in hepatic stellate cells (HSCs) and epithelial-mesenchymal transition (EMT) of hepatocytes.    Methods  Quantitative RT-PCR was used to determine miR-21 and the expression of  SPRY2, HNF4α  and other genes. Immunoblotting assay was carried out to examine the expression of relevant proteins. Luciferase reporter assay was performed to assess the effects of miR-21 on its predicted target genes  SPRY2  and  HNF4α . Primary HSCs and hepatocytes were treated with miR-21 mimics/inhibitors or appropriate adenoviral vectors to examine the relation between miR-21 and  SPRY2  or  HNF4α.Results  The serum and hepatic content of miR-21 was significantly higher in cirrhotic patients and rats.  SPRY2  and  HNF4α  mRNA levels were markedly lower in the cirrhotic liver. MiR-21 overexpression was associated with enhanced ERK1 signaling and EMT in liver fibrosis. Luciferase assay revealed suppressed  SPRY2  and  HNF4α  expression by miR-21. Ectopic miR-21 stimulated ERK1 signaling in HSCs and induced hepatocyte EMT by targeting  SPRY2  or  HNF4α . Downregulating miR-21 suppressed ERK1 signaling, inhibited HSC activation, and blocked EMT in TGFβ1-treated hepatocytes.    Conclusions  MiR-21 modulates ERK1 signaling and EMT in liver fibrosis by regulating  SPRY2  and  HNF4α  expression. MiR-21 may serve as a potentially biomarker as well as intervention target for hepatic cirrhosis.

MiR-21 Simultaneously Regulates ERK1 Signaling in HSC Activation and Hepatocyte EMT in Hepatic Fibrosis