Yu Shengyou1, Yu Li2. 1. Department of Pediatrics, Guangzhou First People's Hospital, affiliate to Guangzhou Medical University, China. 2. Department of Pediatrics, Guangzhou First People's Hospital, affiliate to Guangzhou Medical University, China yuli828@yeah.net.
Abstract
OBJECTIVE: the objective of this article is to evaluate the role of siRNA-silenced TRPC6 on podocyte autophagy and apoptosis induced by AngII. METHODS: mouse podocyte cell lines were cultured in vitro. The apoptosis rates of each group were detected using flow cytometry. The expression of LC3-II protein and changes in distribution were detected by confocal laser, and the western blot protocol was employed for detection of protein expression of LC3-II. RESULTS: AngII-injured podocyte had a significant increase in apoptosis, while silencing TRPC6 could decrease the apoptosis induced by AngII. Autophagy remarkably increased after AngII injury. While silencing TRPC6 stabilized the autophagy expression, AngII could activate the autophagy of podocyte. Autophagy-associated protein LC3-II expression increased after AngII injury. The LC3-II mRNA and the protein level could be down regulated by 3-MA. The silencing of TRPC6 could stabilize the autophagy expression. CONCLUSION: the data suggest that AngII can lead to podocyte injury. Autophagy may have beneficial effects in preventing the progression of proteinuria. This study provides some new clues for further exploring the occurrence of podocyte injury and the development mechanism of proteinuria.
OBJECTIVE: the objective of this article is to evaluate the role of siRNA-silenced TRPC6 on podocyte autophagy and apoptosis induced by AngII. METHODS:mouse podocyte cell lines were cultured in vitro. The apoptosis rates of each group were detected using flow cytometry. The expression of LC3-II protein and changes in distribution were detected by confocal laser, and the western blot protocol was employed for detection of protein expression of LC3-II. RESULTS:AngII-injured podocyte had a significant increase in apoptosis, while silencing TRPC6 could decrease the apoptosis induced by AngII. Autophagy remarkably increased after AngII injury. While silencing TRPC6 stabilized the autophagy expression, AngII could activate the autophagy of podocyte. Autophagy-associated protein LC3-II expression increased after AngII injury. The LC3-II mRNA and the protein level could be down regulated by 3-MA. The silencing of TRPC6 could stabilize the autophagy expression. CONCLUSION: the data suggest that AngII can lead to podocyte injury. Autophagy may have beneficial effects in preventing the progression of proteinuria. This study provides some new clues for further exploring the occurrence of podocyte injury and the development mechanism of proteinuria.