Abstract

This study aims to identify potential microRNAs (miRNAs) contribute to liver fibrosis progression and investigate how the miRNA is involved. We recruited totally 58 patients. Magnetic resonance imaging was employed to detect fibrosis. Classification of liver fibrosis was carried out by Ishak scoring system. Cell viability was tested using cell counting kit-8. Measurements of mRNA and protein expressions were conducted using real-time quantitative polymerase chain reaction and western blotting. Luciferase reporter assay was recruited for determination of miR-29b-3p targets. We found that relative enhancement (RE) values were reduced with the increases in fibrosis stages and was negatively associated with Ishak scores. In comparison with patients without liver fibrosis, miR-29b-3p level was remarkably reduced in those with liver fibrosis. Its level was found to be positively associated with RE values. Transforming growth factor beta 1 (TGF-β1)-induced hepatic stellate cell (HSC) activation significantly decreased miR-29b-3p expression. However, miR-29b-3p overexpression repressed TGF-β1-induced collagen I protein and alpha-smooth muscle actin (α-SMA) expression. As expected, its overexpression also reduced cell viability. We found that miR-29b-3p directly bind to signal transducer and activator of transcription 3 (STAT3) and suppressed its expression. Our study demonstrates that low expression of miR-29b-3p may contribute to the progression of liver fibrosis by suppressing STAT3.

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