Published online Aug 21, 2019. doi: 10.3748/wjg.v25.i31.4468
Peer-review started: March 29, 2019
First decision: June 10, 2019
Revised: June 25, 2019
Accepted: July 19, 2019
Article in press: July 19, 2019
Published online: August 21, 2019
Processing time: 145 Days and 17.4 Hours
Activation of hepatic stellate cells (HSCs) is a pivotal event in the onset and progression of liver fibrosis. Loss of microRNA-194 (miR-194) has been reported in activated HSCs, but the actual role of miR-194 in liver fibrosis remains uncertain.
To explore the role and potential mechanism of miR-194-mediated regulation of liver fibrosis in vitro and in vivo.
The expression of miR-194 was examined in human fibrotic liver tissues, activated HSCs, and a carbon tetrachloride (CCl4) mouse model by qPCR. The effects of AKT2 regulation by miR-194 on the activation and proliferation of HSCs were assessed in vitro. For in vivo experiments, we reintroduced miR-194 in mice using a miR-194 agomir to investigate the functions of miR-194 in liver fibrosis.
MiR-194 expression was notably lacking in activated HSCs from both humans and mice. Overexpression of miR-194 (OV-miR-194) inhibited α-smooth muscle actin (α-SMA) and type I collagen (Col I) expression and suppressed cell proliferation in HSCs by causing cell cycle arrest in G0/G1 phase. AKT2 was predicted to be a target of miR-194. Notably, the effects of miR-194 knockdown in HSCs were almost blocked by AKT2 deletion, indicating that miR-194 plays a role in HSCs via regulation of AKT2. Finally, miR-194 agomir treatment dramatically ameliorated liver fibrosis in CCl4-treated mice.
We revealed that miR-194 plays a protective role by inhibiting the activation and proliferation of HSCs via AKT2 suppression. Our results further propose miR-194 as a potential therapeutic target for liver fibrosis.
Core tip: The expression of miR-194 was significantly downregulated in activated primary hepatic stellate cells (HSCs) from CCl4-treated mice, TGF-β1-treated LX2 cells, and the liver of advanced fibrosis patients. MiR-194 significantly inhibited the expression of α-SMA, Col I, and cyclin D1 and suppressed the activation and proliferation of HSCs in vitro by repressing AKT2 signaling. MiR-194 could attenuate liver fibrosis progression to some extent in a mouse model. Reintroduction of miR-194 offered a possible therapeutic approach for ameliorating liver fibrosis.