Rab8A调节C2C12成肌细胞中胰岛素刺激的GLUT4转位。
Rab8A regulates insulin-stimulated GLUT4 translocation in C2C12 myoblasts.
作者信息
Li Hanbing, Ou Liting, Fan Jiannan, Xiao Mei, Kuang Cuifang, Liu Xu, Sun Yonghong, Xu Yingke
机构信息
Department of Biomedical Engineering, Key Laboratory for Biomedical Engineering of Ministry of Education, Zhejiang Provincial Key Laboratory of Cardio-Cerebral Vascular Detection Technology and Medicinal Effectiveness Appraisal, Zhejiang University, Hangzhou, China.
College of Pharmaceutical Science, Zhejiang University of Technology, Hangzhou, China.
出版信息
FEBS Lett. 2017 Feb;591(3):491-499. doi: 10.1002/1873-3468.12555. Epub 2017 Jan 30.
Rab proteins are important regulators of GLUT4 trafficking in muscle and adipose cells. It is still unclear which Rabs are involved in insulin-stimulated GLUT4 translocation in C2C12 myoblasts. In this study, we detect the colocalization of Rab8A with GLUT4 and the presence of Rab8A at vesicle exocytic sites by TIRFM imaging. Overexpression of dominant-negative Rab8A (T22N) diminishes insulin-stimulated GLUT4 translocation, while constitutively active Rab8A (Q67L) augments it. In addition, knockdown of Rab8A inhibits insulin-stimulated GLUT4 translocation, which is rescued by replenishment of RNAi-resistant Rab8A. Together, these results indicate an indispensable role for Rab8A in insulin-regulated GLUT4 trafficking in C2C12 cells.
Rab蛋白是肌肉和脂肪细胞中GLUT4转运的重要调节因子。目前尚不清楚哪些Rab蛋白参与C2C12成肌细胞中胰岛素刺激的GLUT4易位。在本研究中，我们通过全内反射荧光显微镜（TIRFM）成像检测Rab8A与GLUT4的共定位以及Rab8A在囊泡胞吐位点的存在。显性负性Rab8A（T22N）的过表达减少了胰岛素刺激的GLUT4易位，而组成型活性Rab8A（Q67L）则增强了这种易位。此外，Rab8A的敲低抑制了胰岛素刺激的GLUT4易位，而通过补充RNAi抗性Rab8A可挽救这种抑制作用。总之，这些结果表明Rab8A在C2C12细胞中胰岛素调节的GLUT4转运中起不可或缺的作用。
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