Abstract: Objective To explore the role and mechanisms of miR-17-5p in the pathogenesis of childhood nephrotic syndrome. Methods miR-17-5p mimic were transfected into podocytes in kidney of mice (MPC5) for 24 h to harvest the cells. the potential targets of MiR-117-5P were searched using the prediction programs microRNA.org, TargetScan and PicTar. RT-PCR and Western blot were used to detect expression of PTPRO mRNA and protein. Ca2+ fluorescence indicator with Fluo-3-Amspecificity were used to measure intracellular free calcium concentration ([Ca2+]i) in podocytes. Annexin V/PI flow cytomeutry was used to test apoptosis rate of podocytes. Results According to the bioinformatics technology prediction, miR-17-5p derived from human or mouse all can bind to multiple sites of the corresponding PTPRO-3 'UTR region and inhibit the expression of PTPRO protein and mRNA. PTPRO overexpression inhibits miR-17-5p-induced increase of [Ca2+]i in podocytes in kidney of mice. PTPRO overexpression alleviates miR-17-5p-induced apoptosis of podocytes in kidney of mice. Conclusion miR-17-5p inhibits expression of PTPRO in podocytes in kidney of mice and stimulates increase of intracellular free calcium concentration ([Ca2+]i) in podocytes, inducing apoptosis of podocytes in kidney of mice.

Key words: MiR-17-5p, glomerular epithelial protein 1, glomerular podocytes, apoptosis