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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&lt;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.

TRPC6 May Protect Renal Ischemia-Reperfusion Injury Through Inhibiting Necroptosis of Renal Tubular Epithelial Cells