胰岛素通过PI3K通路上调大鼠血管平滑肌细胞KCa3.1通道
Insulin upregulation of KCa3.1 channels via PI3K pathway in rat vascular smooth muscle cells
目的：观察胰岛素对血管平滑肌细胞（vascular smooth muscle cells, VSMCs）中电导钙激活钾通道（intermediate-conductance Ca2+-activated K+ channels, KCa3.1）的影响及与PI3K信号通路的关系。方法：体外培养大鼠胸主动脉平滑肌细胞，应用全细胞膜片钳、逆转录聚合酶链反应（RT-PCR）和免疫细胞化学方法观察KCa3.1电流和表达的变化；应用MTT法观察VSMCs增殖；应用细胞划痕和改良boyden小室法观察VSMCs迁移。结果：1 μM胰岛素与VSMCs孵育24 h导致KCa3.1电流幅度增大，KCa3.1在mRNA和蛋白水平的表达均明显增强，该效应可被PI3K信号通路阻断剂LY294002抑制。1 μM胰岛素促进VSMCs迁移、增殖，此作用可被KCa3.1特异性阻断剂TRAM-34及LY294002抑制。结论：胰岛素通过PI3K信号通路上调KCa3.1通道表达，促进VSMCs的迁移和增殖。
ims- The present study was designed to investigate whether insulin regulates KCa3.1 channels in vascular smooth muscle cells (VSMCs) via PI3K signal pathway. Methods- Cultured VSMCs were employed to investigate the regulation of KCa3.1 channels by insulin and roles of KCa3.1 channels in cell migration and proliferation using approaches of electrophysiology and molecular biology. Results- KCa3.1 channel mRNA and protein levels, and current density were greatly enhanced in cultured VSMCs treated with 1 μM insulin, and the effects were countered in the cells treated with the PI3K inhibitor LY294002. In addition, insulin stimulated cell migration and proliferation in cultured VSMCs, and the effects were fully reversed in the cells treated with the KCa3.1 blocker TRAM-34 or LY294002. Conclusions- These results demonstrate the novel information that insulin increases expression of KCa3.1 channels via PI3K patyway and therefore promotes migration and proliferation of VMSCs, which likely play a role at least in part in the development of vasculopathy in type-2 diabetes.
苏兴利、王燕、王亚文、邓秀玲
基础医学生理学细胞生物学
血管平滑肌细胞中电导钙激活钾通道胰岛素PI3K
intermediate-conductance Ca2+ activated K+ channelinsulinVSMCsPI3K
苏兴利,王燕,王亚文,邓秀玲.胰岛素通过PI3K通路上调大鼠血管平滑肌细胞KCa3.1通道[EB/OL].(2011-06-21)[2025-08-16].http://www.paper.edu.cn/releasepaper/content/201106-384.点此复制
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