TRPC6在高糖所致足细胞骨架F-actin损伤中的作用

The role of TRPC6 in high glucose-induced podocytes F-actin injury

目的探讨瞬时受体电位阳离子通道6(Transient receptor potential canonical channel 6,TRPC6)在高糖诱导的肾小球足细胞骨架纤维状肌动蛋白(F-actin)损伤中的作用。方法以条件永生性人类肾小球足细胞为研究对象,分别采用Real-time PCR,Western blot技术观察高糖条件下足细胞TRPC6mRNA和蛋白表达的变化,通过激光共聚焦法观察高糖作用下足细胞内钙的变化,以及利用激光共聚焦检测技术观察高糖条件下足细胞F-actin变化。结果 Real-time PCR和Western blot实验显示高糖作用下足细胞TRPC6通道蛋白mRNA和蛋白表达明显上调;共聚焦数据显示,高糖作用下足细胞内钙明显增多,高糖条件下足细胞F-actin出现重构,使用TRPC6抑制剂后有所恢复。结论高糖诱导足细胞骨架F-actin发生损伤,且TRPC6参与高糖所致的足细胞骨架F-actin损伤。

Objective To investigate the role of transient receptor potential canonical channel 6（TRPC6） in glomerular podocytes F-actin injury induced by high glucose. Methods The conditionally immortalized human glomerular podocytes were cultured and the injury was in- duced by high glucose. Real-time PCR, Western blot and laser scanning confocal microscope were used to detect the alteration of TRPC6 mRNA, TRPC6 protein, calcium influx and podo- cytes F-actin under high glucose, respectively. Results After mRNA, protein of TRPC6 and calcium influx were up-regulated high glucose stimulation, the significantly ; laser scanning confocal microscope experiments showed that high glucose induced podocytes F-actin reorgani- zation which recovered in part after using TRPC6 inhibitor. Condusion TRPC6 is involved in high glucose-induced podocytes F-actin injury.