坏死性下垂
TRPC6型
转染
细胞凋亡
程序性细胞死亡
肾缺血
细胞生物学
再灌注损伤
化学
生物
癌症研究
分子生物学
缺血
医学
细胞培养
生物化学
内科学
受体
瞬时受体电位通道
遗传学
作者
Bingbing Shen,Yue He,Shan Zhou,Hongwen Zhao,Mei Mei,Xiongfei Wu
出处
期刊:Medical Science Monitor
[International Scientific Information, Inc.]
日期:2016-02-25
卷期号:22: 633-641
被引量:20
摘要
BACKGROUND The aim of this study was to explore the potential role of TRPC6 in the pathophysiology of HK-2 cell injury following ischemia reperfusion (I/R). MATERIAL AND METHODS TRPC6 expression was analyzed by immunofluorescence staining. siRNA was transfected to knockout of TRPC6 in HK-2 cells, and in vitro I/R was then induced. Cell apoptosis and necrosis were determined by Annexin V-FITC/PI staining. Necroptosis was determined by necrostatin-1 and expressions of necroptosis-related proteins were evaluated. OAG, SKF96365, or KN-93 was further used to interfere with TRPC6 expression. RESULTS Cytoplasmic TRPC6 expression was demonstrated. I/R induced TRPC6 expression in normal or NC siRNA-transfected cells but not in TRPC6 siRNA-knockout ones. There was a progressive increase in apoptotic and necrotic cells with increasing reoxygenation time in all 3 groups, while necrosis in TRPC6 siRNA-transfected cells was comparatively higher than that of the other 2 groups (p<0.05). Expressions of necroptosis-related proteins were interfered with following I/R and these effects were enhanced by TRPC6 siRNA. Application of OAG, SKF96365, or KN93 further affected necroptosis following I/R. CONCLUSIONS This study described the expression and functional relevance of TRPC6 in the pathophysiology of HK-2 cell following I/R. Our results regarding the ability of TRPC6 to specifically interrupt necroptosis may shed new light on its role in prevention and control of ischemic kidney injury.
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