血流剪切应力刺激后人脐带内皮细胞HIAP-2的表达

目的:阐明血流剪切应力抑制血管内皮细胞凋亡的分子机制.方法:人脐静脉内皮细胞(HUVECs)培养于DMEM,细胞融合时将细胞暴露于2 N/m2的剪切应力,分别用Nortern blot及Western blot法检测人凋亡抑制蛋白2(HIAP-2)mRNA及蛋白的表达.结果:HUVECs在静止状态下表达少量HIAP-2mRNA及蛋白,在2N/m2的剪切应力2～6 h刺激下可诱导HUVECs产生HIAP-2mRNA,且量明显增加.HIAP-2蛋白在2 N/m2剪切应力4～24 h刺激下表达明显增加.结论:生理水平剪切应力能够明显诱导内皮细胞产生HIAP-2mRNA和蛋白的表达,可能是剪切应力抑制内皮细胞凋亡发挥抗动脉粥样硬化作用的机制之一.

Expression of HIAP-2 in human umbilical vein endothelial cells after shear stress

Objective: To investigate the molecular mechanisms in regulating shear stress-mediated inhibition of apoptosis. Methods:Human umbilical vein endothelial cells (HUVECs) were cultured and passaged in DMEM. The cells were exposed to laminar shear stress at 2 N/m 2 after fusion. The expressions of the human inhibitor of apoptosis protein-2(HIAP-2)mRNA and protein in HUVECs were determined by Northern blotting and Western blotting. Results:A small amount of HIAP-2 mRNA and protein expressed at static condition.The laminar shear stress at 2 N/m 2 for 2 to 6 hours stimulated HUVECs to express much more HIAP-2 mRNA. Expression of HIAP-2 protein was also significantly increased at 2 N/m 2 of shear stress for 4 to 24 hours. Conclusion:Laminar shear stress at physiological level induces significant expressions of HIAP-2 mRNA and protein. Up-regulation of HIAP-2 may contribute to the potent antiatherosclerotic effect of shear stress by preventing endothelial cells from apoptosis.