Angâ…¡-NFAT-TRPC6Signaling Pathway Mediates High Glucose Induced Podocyte Injury

Objective:To investigate the expression of canonical transient receptor potential cation channel6(TRPC6) of mouse podocytes induced by high glucose, and to explore its possible mechanism.Method:Mouse podocyte cell line was cultured and divided into normal control groups, which include normal glucose group (NG), mannitol group (HM), high glucose group (HG), U73122control group (HU), valsartan treatment groups,which contains HG+low dose of valsartan treatment group (LV) and HG+high dose of valsartan treatment group (HV). After48hours,the expressions of mRNA and proteins of TRPC6, NFAT2, nephrin were detected respectively by real-time quantitative PCR and Western blot analysis;the apoptosis rate of podocytes was detected by flow cytometry.Result:Compared with control group,the expressions of TRPC6, NFAT2, AngⅡ were significantly elevated in HG group (P＜0.05), while the expression of nephrin was decreased (P＜0.05). TRPC6, NFAT2AngⅡ expressions were markedly downregulated by valsartan (P＜0.05), while nephrin expressions were effectively upregulated (P＜0.05), and the effect of the high dose of valsartan was more significantly. Compared with HG group, the expressions of TRPC6and NFAT2were decreased in HU group,and the expressions of TRPC6, NFAT2, nephrin AngⅡhad no statistical significance between NG group and HM group (P＞0.05).Conclusions:angiotensin receptor antagonist can protect podocytes induced by high glucose by attenuate TRPC6expression via AngII-NFAT-TRPC6signaling pathway.