天津医药

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CaMK II在收缩促进骨骼肌细胞GLUT4转位中的作用

于俊娜1,牛文彦2,3   

  1. 1. 天津医科大学
    2. 天津医科大学免疫教研室
    3.
  • 收稿日期:2010-12-22 修回日期:2011-01-11 出版日期:2011-06-15 发布日期:2011-06-15
  • 通讯作者: 于俊娜

The Role of CaMK II in Contraction-stimulated GLUT4 Translocation in Skeletal Muscle Cells

Jun-Na YU 2,2   

  • Received:2010-12-22 Revised:2011-01-11 Published:2011-06-15 Online:2011-06-15
  • Contact: Jun-Na YU

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摘要： 摘要 目的：探讨钙/钙调蛋白依赖性蛋白激酶II（CaMK II）在收缩促进GLUT4转位机制中的作用。方法：将接种在培养板中的C2C12GLUT4myc骨骼肌细胞分为对照组和carbachol（乙酰胆碱受体激动剂）组，两组均分别用CaMK II的特异性抑制剂KN93或KN62预孵育，用酶联免疫吸附法（ELISA）测定细胞膜上GLUT4myc的含量（转位）；用KN93预孵育后，免疫印迹法测定蛋白激酶CaMK II的磷酸化。结果：KN93和KN62抑制carbachol刺激的GLUT4myc转位；carbachol磷酸化CaMK II，KN93抑制此作用。结论：CaMK II位于Ca2＋下游介导收缩促进GLUT4myc 转位的作用。

关键词: CaMK II, 肌, 骨骼, 葡萄糖转运子4, Carbachol, 收缩

Abstract: Abstract Objective: To study the role of Ca2＋/Calmodulin- dependent protein kinase II (CaMK II) in the mechanism of contract-stimulated glucose transport 4 translocation in skeletal muscle cells. Methods: C2C12GLUT4myc myotubes were divided into two groups with or without carbachol (acetylcholine receptor agonist) treatment. CaMK II inhibitor KN93 or KN62 was added to the medium prior to treatment, respectively. Then cell surface levels of GLUT4myc were measured by enzyme linked immunosorbent assay (ELISA). The phosphorylation of CaMK II was detected by immunoblotting after pre-incubation with KN93 before treatment. Results: Carbachol increased phosphorylation of CaMK II which was reduced by KN93. KN93 and KN62 inhibited the gain of cell surface GLUT4myc induced by Cch. Conclusion: CaMK II is the downstream signal of Ca2＋ and mediates contraction-stimulated GLUT4myc traffic in skeletal muscle cells.

Key words: CaMK II, muscle, skeletal, GLUT4, carbachol, contraction