In our previous study, miR-126 was identified as one of the leading miRNAs that is downregulated during activation of hepatic stellate cells (HSCs). However, the roles and related mechanisms of miR-126 in HSCs are not understood. In this study, we compared expression of miR-126 during HSC activation both in vitro and in vivo. We also applied RNA interference to analyze the role and mechanism of miR-126(*) in the activation of HSCs. Restoring HSCs with Lv-miR-126(*) resulted in decreased proliferation, accumulation of extracellular matrix components, and cell contraction, while also negatively regulating the vascular endothelial growth factor (VEGF) signal transduction pathways by partially targeted VEGF-A. Thus, we postulate that miR-126 may be a biological marker for the activation of HSCs, and useful for reducing intrahepatic vascular resistance and improving the sinusoidal microcirculation in chronic liver diseases.
Keywords: 3′UTR; 3′untranslated region; Akt; COL IV; Chronic liver disease; ECM; EGFL7; GO; HA; HE; HSC; Hepatic stellate cell; KEGG; LN; PCIII; PI3K; Portal hypertension; VEGF; VEGFA; VG; Van Gieson; epidermal growth factor-1ike domain 7; extracellular matrix; gene ontology; hematoxylin/eosin; hepatic stellate cell; hyalaronic acid; kyoto encyclopedia of genes and genomes; laminin; miR-126(∗); miRNA; microRNA; phosphatidylinositol-3-kinase; procollagen typeIII; protein kinase B; type IV collagen; vascular endothelial growth factor.
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