Published online Sep 14, 2015. doi: 10.3748/wjg.v21.i34.9900
Peer-review started: February 27, 2015
First decision: March 26, 2015
Revised: April 11, 2015
Accepted: July 3, 2015
Article in press: July 3, 2015
Published online: September 14, 2015
Processing time: 200 Days and 4.7 Hours
AIM: To reveal the functions of microRNAs (miRNAs) with respect to hepatic stellate cells (HSCs) in response to portal hypertension.
METHODS: Primary rat HSCs were exposed to static water pressure (10 mmHg, 1 h) and the pressure-induced miRNA expression profile was detected by next-generation sequencing. Quantitative real-time polymerase chain reaction was used to verify the expression of miRNAs. A potential target of MiR-9a-5p was measured by a luciferase reporter assay and Western blot. CCK-8 assay and Transwell assay were used to detect the proliferation and migration of HSCs under pressure.
RESULTS: According to the profile, the expression of miR-9a-5p was further confirmed to be significantly increased after pressure overload in HSCs (3.70 ± 0.61 vs 0.97 ± 0.15, P = 0.0226), which resulted in the proliferation, migration and activation of HSCs. In vivo, the up-regulation of miR-9a-5p (2.09 ± 0.91 vs 4.27 ± 1.74, P = 0.0025) and the down-regulation of Sirt1 (2.41 ± 0.51 vs 1.13 ± 0.11, P = 0.0006) were observed in rat fibrotic liver with portal hypertension. Sirt1 was a potential target gene of miR-9a-5p. Through restoring the expression of Sirt1 in miR-9a-5p transfected HSCs on pressure overload, we found that overexpression of Sirt1 could partially abrogate the miR-9a-5p mediated suppression of the proliferation, migration and activation of HSCs.
CONCLUSION: Our results suggest that during liver fibrosis, portal hypertension may induce the proliferation, migration and activation of HSCs through the up-regulation of miR-9a-5p, which targets Sirt1.
Core tip: Portal hypertension is a syndrome as the main characteristics of the portal system hemodynamics change. Hepatic stellate cell (HSC) activation is the key factor of promoting the development of the occurrence of liver cirrhosis and portal hypertension. We determined the levels of miR-9a-5p in HSCs under pressure. We found that higher levels of miR-9a-5p, which targeted Sirt1, were expressed in vivo. The restored expression of miR-9a-5p and Sirt1 could significantly suppress the proliferation, migration and activation of HSCs.