MiR-150-5p Alleviates Renal Tubular Epithelial Cell Fibrosis by Activating Autophagy via β-catenin Signaling

To verify whether miR-150-5p modulates the development of renal fibrosis and its mechanism.

Transforming growth factor (TGF)-β1 was implemented on HK-2 cells to construct a renal fibrosis in vitro model. Inhibition of autophagy was performed on HK-2 cells by treating with 3-methyladenine (3-MA, an inhibitor of autophagy). HK-2 cells experienced transfection by miR-150-5p mimics/inhibitor and pcDNA-β-catenin plasmids, and the negative controls. Dual luciferase reporter gene assay was applied to validate the relationship between miR-150-5p and β-catenin. Cell apoptosis exploration was implemented by flow cytometry assay. The level detection of CoII, α-SMA, miR-150-5p and β-catenin was executed by real-time quantitative reverse transcription-polymerase chain reaction. The expression of CoII, α-SMA, LC3I, LC3II, Bax, Cleaved Caspase 3, Beclin 1, Bcl-2 and β-catenin proteins was monitored by western blot.

Autophagy was inhibited in TGF-β1-induced HK-2 cells. MiR-150-5p alleviated fibrosis, enhanced autophagy, and inhibited apoptosis in TGF-β1-induced HK-2 cells. β-catenin was a target of miR-150-5p. Autophagy inhibition or β-catenin partially counteracted miR-150-5p effect on TGF-β1-induced fibrosis in HK-2 cells.

MiR-150-5p alleviates renal tubular epithelial cell fibrosis by activating autophagy via β-catenin signaling.