机械张应变诱导蛋白激酶B活化对血管平滑肌细胞迁移的影响  

Effect of Akt/PKB activation on mechanical strain-induced vascular smooth muscle cell migration

作　　者：朱妤[1] 严志强[1] 沈宝荣[1] 姜宗来[1] 

机构地区：[1]上海交通大学力学生物学与医学工程实验室,上海200240

出　　处：《医用生物力学》2006年第4期259-261,266,共4页Journal of Medical Biomechanics

基　　金：国家自然科学基金资助项目(10472071;10132020)

摘　　要：目的研究机械张应变诱导蛋白激酶B活化对大鼠血管平滑肌细胞迁移能力的影响。方法应用FX-4000T细胞应变加载系统,对大鼠血管平滑肌细胞施加牵拉幅度为15%、频率为1Hz的张应变。以Transwell和Westernblot等方法观察张应变作用下蛋白激酶B磷酸化和血管平滑肌细胞迁移能力的变化,以未加载张应变的血管平滑肌细胞为对照组。结果与对照组相比,机械张应变增加细胞中蛋白激酶B磷酸化水平,促进血管平滑肌细胞的迁移;PI3K的特异性抑制剂Wortmannin抑制张应变诱导的蛋白激酶B的磷酸化,降低了血管平滑肌细胞迁移能力。结论机械张应变通过上调蛋白激酶B磷酸化水平促进了血管平滑肌细胞迁移,提示蛋白激酶B信号通路参与机械张应变条件下血管平滑肌细胞迁移过程的信号传导。Objective To investigate the role of Akt/PKB activation induced by mechanical strain on vascular smooth muscle cell （VSMC） migration. Methods VSMCs of rat aorta were subjected tocyclic tensile strain （15%, 1 Hz） by using a FX-4000T system, with VSMCs in static conditions as a control. VSMC migration and the phosphorylation of Akt/PKB were examined by Transwell assay and Western blot. Results Tensile strain （15%, 1Hz） obviously enhanced both VSMC migration and Akt/PKB activation compared with the control. While Wortmannin, a specific inhibitor of phosphatidylinositol-3 kinase, can attenuate the phosphorylation of Akt/PKB stimulated by the strain so as to reduce VSMC migration. Conclusion Akt/PKB activation could be enhanced by tensile strain to promote VSMC migration, and Akt/PKB involved in such VSMC migration via PI3K-Akt/PKB signaling pathway.

关 键 词：机械张应变 血管平滑肌细胞 细胞迁移 蛋白激酶B 

分 类 号：R318.01[医药卫生—生物医学工程]