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BioMed Research International
Volume 2017, Article ID 1945631, 12 pages
Research Article

MicroRNA-195 Activates Hepatic Stellate Cells In Vitro by Targeting Smad7

1Department of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China
2Department of Pharmacy, Shaoxing Seventh People’s Hospital, Shaoxing, Zhejiang, China

Correspondence should be addressed to Shi-Kun Liu; moc.621@6948168l

Received 9 April 2017; Revised 3 July 2017; Accepted 26 July 2017; Published 27 August 2017

Academic Editor: Gulam Waris

Copyright © 2017 Li-Ying Song et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background and Aim. Aberrant activation of the TGF-β1/Smad pathway contributes to the activation of hepatic stellate cells (HSCs). MicroRNA-195 has been shown to regulate the activation of HSCs. The aim of this study was to investigate the role of miRNA-195 in HSCs activation. Methods. A liver fibrotic rat model induced by diethylnitrosamine was established. Dual luciferase reporter assays were performed to verify that Smad7 was the target of miRNA-195. The expression levels of miR-195, Smad7, and α-SMA in HSC-T6 transfected, respectively, with miR-195 mimic, inhibitor, or control were measured by qRT-PCR. The protein expression of Smad7 was detected by Western blot analysis. Results. Enhanced miR-195 and decreased Smad7 were observed in diethylnitrosamine-induced liver fibrotic rats (). Dual luciferase reporter assays showed that the miR-195 mimic significantly suppressed the luciferase activity of a reporter plasmid carrying the binding site of miR-195 on the 3′UTR of Smad7 (). The miR-195 mimics activated HSCs, further elevated miR-195 and α-SMA (), and reduced the Smad7 level (). The miR-195 inhibitors blocked the activation of HSCs, reduced the expression of miR-195 and -SMA (), and upregulated the expression of Smad7 (). Conclusion. Collectively, we demonstrated that miRNA-195 activated HSCs by targeting Smad7.