胰岛素经PI3K/Akt/p70S6K1信号通路促进小鼠成肌细胞的增殖(1)
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(上海第十人民医院 上海 20072)
【摘要】目的：探讨在促小鼠成肌细胞增殖过程中，胰岛素对PI3K/Akt/p70S6K1信号传导通路的作用。方法：以小鼠成肌细胞C2C12为研究对象，利用蛋白免疫印迹(western blot)和MTT方法检测Akt蛋白激酶的表达和细胞增殖变化。结果(1)胰岛素(100-200 nM)浓度依赖性地促进C2C12细胞的增殖，胰岛素干预C2C12细胞，引起Akt/p70S6K1的磷酸化；(2)PI3K抑制剂LY294002能浓度依赖地抑制胰岛素引起的Akt磷酸化和细胞增殖；(3)p70S6K1抑制剂—雷帕霉素(rapamycin) 浓度依赖地抑制胰岛素引起的p70S6K1磷酸化和细胞增殖。结论：胰岛素促进小鼠C2C12成肌细胞的增殖。胰岛素能激活C2C12细胞的Akt/p70S6K1信号通路，并且这种激活是胰岛素促进的C2C12细胞增殖所必需的。
【关键词】胰岛素；C2C12细胞；Akt/p70S6K1的磷酸化；雷帕霉素
InsulinpromoteC2C12 myoblast proliferation viaPI3K/Akt/p70S6K1
Mei Aihong1 Yan Zhengmao1 Zhang Guoliang1 Wu Guoting2
【Abstract】Objective: To explore the effectof insulin in on the signaling pathway of PI3K/Akt/p70S6K1 related to the myoblasts proliferation of rats.Methods:, western blotwasperformed to detect the protein expression in cultured mouse C2C12 myoblasts.Results: (1) Insulin (100-200 nM) can stimulateC2C12 myoblasts proliferation with a dose dependent manner andpromotethe phosphorylation of Akt/p70S6K1. (2) PI3K inhibitor of LY294002 can inhibit insulin-induced Akt phosphorylation and cell proliferation with a concentration dependent manner. (3) p70S6K1 inhibitor of rapamycin can inhibit insulin-induced p70S6K1 phosphorylation and cell proliferation with a concentration relationship . Conclusion:. Insulin can stimulate C2C12 myoblast proliferation andthisactivation of Akt/p70S6K1 signaling pathway is necessary for insulin-induced C2C12 myoblast proliferation.
【Key works】Insulin; C2C12; myoblasts;phosphorylation of Akt/p70S6K1;rapamycin
【中图分类号】R711.4【文献标识码】A【文章编号】1008-6455(2011)06-0273-03
骨骼肌损伤后的再生过程包括 ......
(上海第十人民医院 上海 20072)
【摘要】目的：探讨在促小鼠成肌细胞增殖过程中，胰岛素对PI3K/Akt/p70S6K1信号传导通路的作用。方法：以小鼠成肌细胞C2C12为研究对象，利用蛋白免疫印迹(western blot)和MTT方法检测Akt蛋白激酶的表达和细胞增殖变化。结果(1)胰岛素(100-200 nM)浓度依赖性地促进C2C12细胞的增殖，胰岛素干预C2C12细胞，引起Akt/p70S6K1的磷酸化；(2)PI3K抑制剂LY294002能浓度依赖地抑制胰岛素引起的Akt磷酸化和细胞增殖；(3)p70S6K1抑制剂—雷帕霉素(rapamycin) 浓度依赖地抑制胰岛素引起的p70S6K1磷酸化和细胞增殖。结论：胰岛素促进小鼠C2C12成肌细胞的增殖。胰岛素能激活C2C12细胞的Akt/p70S6K1信号通路，并且这种激活是胰岛素促进的C2C12细胞增殖所必需的。
【关键词】胰岛素；C2C12细胞；Akt/p70S6K1的磷酸化；雷帕霉素
InsulinpromoteC2C12 myoblast proliferation viaPI3K/Akt/p70S6K1
Mei Aihong1 Yan Zhengmao1 Zhang Guoliang1 Wu Guoting2
【Abstract】Objective: To explore the effectof insulin in on the signaling pathway of PI3K/Akt/p70S6K1 related to the myoblasts proliferation of rats.Methods:, western blotwasperformed to detect the protein expression in cultured mouse C2C12 myoblasts.Results: (1) Insulin (100-200 nM) can stimulateC2C12 myoblasts proliferation with a dose dependent manner andpromotethe phosphorylation of Akt/p70S6K1. (2) PI3K inhibitor of LY294002 can inhibit insulin-induced Akt phosphorylation and cell proliferation with a concentration dependent manner. (3) p70S6K1 inhibitor of rapamycin can inhibit insulin-induced p70S6K1 phosphorylation and cell proliferation with a concentration relationship . Conclusion:. Insulin can stimulate C2C12 myoblast proliferation andthisactivation of Akt/p70S6K1 signaling pathway is necessary for insulin-induced C2C12 myoblast proliferation.
【Key works】Insulin; C2C12; myoblasts;phosphorylation of Akt/p70S6K1;rapamycin
【中图分类号】R711.4【文献标识码】A【文章编号】1008-6455(2011)06-0273-03
骨骼肌损伤后的再生过程包括 ......
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