MicroRNA-204-3p Attenuates High Glucose-Induced MPC5 Podocytes Apoptosis by Targeting Braykinin B2 Receptor

• Published in: Experimental and clinical endocrinology & diabetes Vol. 127; no. 6; p. 387
• Main Authors: Han, Xu, Li, Qiaobei, Wang, Chunyan, Li, Yinyan
• Format: Journal Article
• Language: English
• Published: Germany 01.06.2019
• Subjects: 3' Untranslated Regions; Animals; Apoptosis - drug effects; Cell Line; Down-Regulation - drug effects; Glucose - pharmacology; Mice; MicroRNAs - metabolism; Podocytes - metabolism; Receptor, Bradykinin B2 - biosynthesis
• ISSN: 1439-3646
• DOI: 10.1055/a-0630-0173

Previous study has been reported that braykinin B2 receptor (Bdkrb2) involves in high glucose-induced renal and podocytes injuries. However, there have been some studies with contradictory results that Bdkrb2 has a protective effect on hyperglycemia-induced injuries in vivo and in vitro. The purpose of the present study was carried out to further investigate the post-transcriptional regulatory mechanism of microRNA (miR) in high glucose-treated podocytes by targeting Bdkrb2 signaling in vitro. The CCK-8 and flow cytometry were performed to measure the cell viability and apoptosis. Gene and protein expression were assayed by RT-qPCR and western blotting, respectively. High glucose treatment decreased cell viability and induced membrane and DNA damage, as well as apoptosis in podocytes. High glucose treatment also increased the expression of Bdkrb2, which was blocked by miR-204-3p mimics transfection in podocytes. Bioinformatics and luciferase reporter activity showed that miR-204-3p was directly targeted to the 3'-untranslated region (3'-UTR) of Bdkrb2. High glucose-induced apoptosis and dysfunction in podocytes were reserved by miR-204-3p mimics transfection, while the effects of miR-204-3p mimics in high glucose-treated podocytes were neutralized by overexpressed Bdkrb2. These findings suggested that miR-204-3p may play a protective role in high glucose-induced apoptosis and dysfunction in podocytes through down-regulation of Bdkrb2.