MiR-17-5p downregulation alleviates apoptosis and fibrosis in high glucose-induced human mesangial cells through inactivation of Wnt/β-catenin signaling by targeting KIF23

Diabetic nephropathy (DN) remains the major cause of end-stage renal disease. MicroRNAs (miRNAs) have been reported to perform biological functions in many diseases. This investigation elucidated the biological role of miR-17-5p in DN. In this study, high glucose-cultured human mesangial cells (HMCs) were used as a cell model of DN. The miR-17-5p and KIF23 expression was measured by RT-qPCR. Cell apoptosis was detected by flow cytometry. The protein levels of apoptosis markers, fibrosis markers, and Wnt/beta-catenin signaling-related genes were assessed using western blotting. The interaction of miR-17-5p with KIF23 was tested by a luciferase reporter assay. We found that miR-17-5p was upregulated in both DN patients and high glucose-treated HMCs. Silencing miR-17-5p attenuated the apoptosis and fibrosis in high glucose-treated HMCs. MiR-17-5p binds to KIF23 3'UTR and negatively regulates KIF23 expression. KIF23 knockdown could suppress the role of miR-17-5p inhibition in high glucose-treated HMCs. Additionally, inhibition of miR-17-5p activated Wnt/beta-catenin signaling in HMCs through upregulating KIF23 expression. Suppression of Wnt/beta-catenin signaling antagonized the effect of miR-17-5p in HMCs. In conclusion, miR-17-5p inhibition alleviates the apoptosis and fibrosis in high glucose-treated HMCs by targeting KIF23 activating Wnt/beta-catenin signaling.