Abstract

This study aimed to investigate the roles of RPSAP52 in renal failure. Our results showed that RPSAP52 was upregulated in plasma of renal failure patients in comparison to healthy controls. Dual luciferase reporter assay showed that RPSAP52 could interact with miR-423-5p, while overexpression of RPSAP52 and miR-423-5p did not alter the expression of each other in human renal proximal tubular epithelial cells (HRPTEpCs). In addition, overexpression of RPSAP52 increased the expression levels of GSTM1 in HRPTEpCs. Cell apoptosis assay showed that overexpression of RPSAP52 and GSTM1 decreased the apoptotic rate of HRPTEpCs under hypoxia conditions. MiR-423-5p played an opposite role and attenuated the effects of overexpressing RPSAP52 and GSTM1. Therefore, RPSAP52 may regulate miR-423-5p/GSTM1 axis to suppress hypoxia-induced HRPTEpC apoptosis.

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