Jing Li1, Xing Fan1, Qian Wang1, Youlan Gong1, Li Guo2. 1. Department of Nephrology, Affiliated Hospital of Hebei University, Baoding, China. 2. Department of Nephrology, Affiliated Hospital of Hebei University, Baoding, China, xq3979@163.com.
Abstract
BACKGROUND/AIMS: This study was designed to examine the role of long noncoding RNA PRNCR1 in cisplatin-induced acute kidney injury (AKI) in vitro and in vivo. METHODS: The expression levels of PRNCR1 and miR-182-5p in cisplatin-induced AKI mice were examined. HK-2 cells were treated with cisplatin to induce cell damage. Then, the effects of PRNCR1 and miR-182-5p on cisplatin-stimulated HK-2 cell viability and apoptosis were detected by the CCK-8 and annexin V-FITC/PI method. Target genes of PRNCR1 and miR-182-5p were analyzed by bioinformatics analysis and luciferase. RESULTS: The expression level of PRNCR1 was significantly reduced in cisplatin-induced AKI mice. In addition, overexpression of PRNCR1 attenuated the damage of cisplatin to HK-2. The expression level of miR-182-5p was significantly raised in cisplatin-induced AKI mice. MiR-182-5p was negatively regulated by PRNCR1 and leaded to an upregulation of EZH1 expression. Overexpression of PRNCR1 attenuated cisplatin-induced apoptosis by downregulating the miR-182-5p/EZH1 axis. CONCLUSION: LncPRNCR1 reduced the apoptosis of renal epithelial cells induced by cisplatin by modulating miR-182-5p/EZH1.
BACKGROUND/AIMS: This study was designed to examine the role of long noncoding RNA PRNCR1 in cisplatin-induced acute kidney injury (AKI) in vitro and in vivo. METHODS: The expression levels of PRNCR1 and miR-182-5p in cisplatin-induced AKI mice were examined. HK-2 cells were treated with cisplatin to induce cell damage. Then, the effects of PRNCR1 and miR-182-5p on cisplatin-stimulated HK-2 cell viability and apoptosis were detected by the CCK-8 and annexin V-FITC/PI method. Target genes of PRNCR1 and miR-182-5p were analyzed by bioinformatics analysis and luciferase. RESULTS: The expression level of PRNCR1 was significantly reduced in cisplatin-induced AKI mice. In addition, overexpression of PRNCR1 attenuated the damage of cisplatin to HK-2. The expression level of miR-182-5p was significantly raised in cisplatin-induced AKI mice. MiR-182-5p was negatively regulated by PRNCR1 and leaded to an upregulation of EZH1 expression. Overexpression of PRNCR1 attenuated cisplatin-induced apoptosis by downregulating the miR-182-5p/EZH1 axis. CONCLUSION: LncPRNCR1 reduced the apoptosis of renal epithelial cells induced by cisplatin by modulating miR-182-5p/EZH1.