摘要
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 2N/m2 的剪切应力 ,分别用Northernblot及Westernblot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~ 6h刺激下可诱导HUVECs产生HIAP 2mRNA ,且量明显增加。HIAP 2蛋白在 2N/m2 剪切应力 4~ 2 4h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。
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.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2004年第4期291-293,共3页
Journal of China Medical University
基金
留学回国人员科研启动基金 ( 1999747)
辽宁省博士启动基金 ( 2 0 0 110 2 0 5 2 )
关键词
内皮细胞
剪切应力
凋亡
endothelial cells
shear stress
apoptosis