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血流剪切应力诱导人脐带内皮细胞HIAP-2的表达
引用本文:金鑫,舒强,凌光烈. 血流剪切应力诱导人脐带内皮细胞HIAP-2的表达[J]. 中国现代医学杂志, 2004, 14(8): 11-14
作者姓名:金鑫  舒强  凌光烈
作者单位:1. 中国医科大学,基础医学院,药理教研室,辽宁,沈阳,110001
2. 中国医科大学,第一附属医院,外科局解教研室,辽宁,沈阳,110001
基金项目:教育部留学回国人员科研启动基金,initia ting fund of Liaoning province for doctors
摘    要:目的生理水平的血流剪切应力有抑制内皮细胞的凋亡等作用进而发挥抗动脉粥样硬化作用,本研究目的是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,当细胞融合时将细胞暴露于20 dyne/cm2的剪切应力,分别用Northern blot及Westem blot法检测human inhibitor of apoptosis protein-2(HIAP-2)mRNA及蛋白的表达.结果 HUVECs在静止状态下表达少量mAP-2mRNA及蛋白,在20 dyne/cm2的剪切应力2~6 h刺激下可诱导HUVECs产生HIAP-2 mR-NA,且量明显增加.HIAP-2蛋白在20 dyne/cm2剪切应力4~24 h刺激下表达明显增加.结论本研究证实生理水平剪切应力能够明显诱导内皮细胞产生HIAP-2 mRNA和蛋白的表达,这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.

关 键 词:内皮细胞  剪切应力  凋亡

Expression of HIAP- 2 in human umbilical vein endothelial cells induced by shear stress
Abstract. Expression of HIAP- 2 in human umbilical vein endothelial cells induced by shear stress[J]. China Journal of Modern Medicine, 2004, 14(8): 11-14
Authors:Abstract
Abstract:Objective: Laminar shear stress at physiological level can inhibit apoptosis of endothelial cells (ECs) and exert a potent antiatheroclerotic effect. The aim of this study is to investigate the molecular mechanisms, which regulate shear stress-mediated inhibition of apoptosis. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured and passaged in DMEM. When the cells became confluent, they were exposed to laminar shear stress at 20 dyne/cm 2. The expressions of the human inhibitor of apoptosis protein-2 (HIAP-2) mRNA and protein were checked by Northem blotting and Westem blotting. Results: HUVECs expressed a small amount of HIAP-2 mRNA and protein at static condition, the laminar shear stress at 20 dyne/cm 2 for 2 to 6 hours stimulated HUVECs to express much more HIAP-2 mRNA. HIAP-2 protein expression was also significantly increased at 20 dyne/cm 2 of shear stress for 4 to 24 hours.Conclusion: The present study provides evidence that 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 on preventing ECs from apoptosis.
Keywords:endothelial cells  shear stress  apoptosis
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