The role of TRPC6 in oxidative stress-induced podocyte ischemic injury.
作者： Bo Zhao , He Yang , Rui Zhang , Hui Sun , Chang Liao
DOI: 10.1016/J.BBRC.2015.04.054
关键词: Actin cytoskeleton 、 Ischemia 、 Downregulation and upregulation 、 TRPC6 、 Gene knockdown 、 Cell biology 、 Hypoxia (medical) 、 Biology 、 Podocyte 、 Oxidative stress
摘要: Increasing evidence suggests that ischemia and hypoxia serve important functions in the development of renal diseases. However, underlying mechanism ischemic injury has not been fully understood. In this study, we found ischemia-reperfusion induced podocyte effacement upregulation TRPC6 mRNA protein expression. in vitro experiments, oxygen glucose deprivation (OGD) treatment enhanced expression TRPC6-dependent Ca2+ influx. knockdown by siRNA interference attenuated OGD-induced [Ca2+]i actin assembly. OGD also increased ROS production. Furthermore, inhibition activity N-acetyl-l-cysteine (NAC) eliminated increase H2O2 treatment, which results oxidative stress, We conclude is involved signaling reorganization podocytes after OGD. These findings provide new insight into mechanisms cellular response to injury.
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