Department of Nephrology, Affiliated Hospital of Hebei University, Baoding, China.
Department of Nephrology, Affiliated Hospital of Hebei University, Baoding, China,
Kidney Blood Press Res. 2021;46(2):162-172. doi: 10.1159/000510157. Epub 2021 Mar 1.
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.
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.
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.
LncPRNCR1 reduced the apoptosis of renal epithelial cells induced by cisplatin by modulating miR-182-5p/EZH1.
背景/目的：本研究旨在探讨长链非编码 RNA PRNCR1 在顺铂诱导的急性肾损伤（AKI）中的作用，分别在体外和体内进行研究。
检测顺铂诱导 AKI 小鼠中 PRNCR1 和 miR-182-5p 的表达水平。用顺铂处理 HK-2 细胞以诱导细胞损伤。然后，通过 CCK-8 和 Annexin V-FITC/PI 法检测 PRNCR1 和 miR-182-5p 对顺铂刺激的 HK-2 细胞活力和凋亡的影响。通过生物信息学分析和荧光素酶检测 PRNCR1 和 miR-182-5p 的靶基因。
PRNCR1 的表达水平在顺铂诱导的 AKI 小鼠中显著降低。此外，过表达 PRNCR1 可减轻顺铂对 HK-2 的损伤。miR-182-5p 在顺铂诱导的 AKI 小鼠中的表达水平显著升高。miR-182-5p 受 PRNCR1 负调控，导致 EZH1 表达上调。过表达 PRNCR1 通过下调 miR-182-5p/EZH1 轴减轻顺铂诱导的细胞凋亡。
LncPRNCR1 通过调节 miR-182-5p/EZH1 减少顺铂诱导的肾上皮细胞凋亡。
