miRNA-150-5p promotes hepatic stellate cell proliferation and sensitizes hepatocyte apoptosis during liver fibrosis

To explore the role of miRNA-150-5p (miR-150-5p) in liver fibrosis. miRNA expression profiles, CCl -induced liver fibrosis progression and regression rodent models, quantitative real-time PCR, miR-150-5p mimics and inhibitors, cell proliferation and apoptosis detection, RNA sequencing and bioinformatics analysis were employed. Liver tissue miR-150-5p expression was positively associated with liver fibrosis progression and regression; however, miR-150-5p exhibited a cell-specific expression pattern, namely, it was enhanced in hepatocytes but reduced in hepatic stellate cells (HSCs) during liver fibrosis; miR-150-5p overexpression promoted HSC apoptosis and sensitized hepatocyte apoptosis; miR-150-5p mimic had a larger influence on the transcriptomic stability of HSCs than that of hepatocytes; miR-150-5p mediated activation of interferon signaling pathways might be responsible for HSC apoptosis. miR-150-5p exhibited an opposite regulation and function pattern between HSCs and hepatocytes during liver fibrosis. miR-150-5p, not as identical as most of others, exhibited a cell-specific expression and function pattern: it was enhanced in hepatocytes but reduced in hepatic stellate cells (HSCs) during liver fibrosis; miR-150-5p overexpression promoted HSC apoptosis and sensitized hepatocyte apoptosis; miR-150-5p silence facilitated HSC proliferation and alleviated hepatocyte apoptosis under the pressure of proapoptotic factors. Taken together, miR-150-5p has potential effects on the pathogenesis of liver fibrosis, but cell-specific targeting carriers should be considered if miR-150-5p is chosen as a therapeutic target for liver fibrosis.