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Shear stress effect on endothelial nitric oxide synthase in cultured human umbilical vein endothelial cells

Shear stress effect on endothelial nitric oxide synthase in cultured human umbilical vein endothelial cells

作     者:Qiuying Gu Dean O. Smith Karlene A. Hoo 

作者机构:Departments of Biological Sciences Texas Tech University Lubbock USA Departments of Chemical Engineering Texas Tech University Lubbock USA 

出 版 物:《Journal of Biomedical Science and Engineering》 (生物医学工程(英文))

年 卷 期:2013年第6卷第10期

页      面:982-986页

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主  题:Shear Stress Endothelial Cells Endothelial Nitric Oxide Synthase Inflammation Thrombosis 

摘      要:Background: Low shear stress caused by disturbed or turbulent flow at arterial branch points is known to associate with atherosclerosis. However, shear stress at the venous valve location and its association with deep vein thrombosis are less understood due to the complex and poorly understood bi-directional flow in the valve pocket region. We investigated how venous endothelial cells respond to flow shear stress around the venous valve region using a novel in vitro system that mimics venous flow. Results: Human umbilical vein EAhy. 926 cells were cultured on a flexible silastic membrane that mimicked venous tissue. Confluent cells were exposed to sinusoidal uni-and bi-directional pulsatile shear stress (0.1 to 1 dyne/cm2) for up to 6 h. Western-blot analyses indicated that endothelial nitric oxide (eNOS) expression levels decreased regardless of all tested flow patterns, stress magnitude, and shearing time. In contrast, the expression levels of inhibitor of κB (kappa B) and α (alpha)-tubulin were unaffected by the shear stress. Conclusions: Our results indicate that shear stress causes a decrease specifically in eNOS expression, suggesting that it may play a significant role in regulating inflammation related protein expression in endothelial cells.

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