microRNA-30c attenuates contrast-induced acute kidney injury by reducing renal tubular epithelial cell apoptosis via targeting SOCS1.

Abstract

Contrast-induced acute kidney injury (CIAKI) is a common complication after contrast media administration. Growing evidences implicate microRNA (miR)-30c has a key role in renal diseases. This study aimed to investigate the role and mechanism of miR-30c in CIAKI. CIAKI rat models were established using tail vein injection of omnipaque. MiR-30c was significantly downregulated in CIAKI models both in vivo and in vitro, concomitant with increased cell apoptosis and deteriorated renal injury. Meanwhile, the cell apoptosis, renal dysfunction and renal injury under contrast exposure were alleviated after overexpression of miR-30c. Mechanistically, we demonstrated that miR-30c directly targeted SOCS1, whose downregulation reduced contrast-induced HK-2 cell apoptosis. Furthermore, the upregulation of SOCS1 abolish the protective effect of the overexpression of miR-30c on contrast-induced cell apoptosis. In summary, overexpression of miR-30c inhibited renal tubular epithelial cell apoptosis and mitigated CIAKI via inhibiting the gene of SOCS1.