Circulation Research. 2002;91:769-775
doi: 10.1161/01.RES.0000038487.19924.18
doi: 10.1161/01.RES.0000038487.19924.18
© 2002 American Heart Association, Inc.
Reviews |
Role of Integrins in Endothelial Mechanosensing of Shear Stress
From the Division of Biomedical Sciences (J.Y.-J.S.), University of California–Riverside, Riverside, Calif, and the Department of Bioengineering and Whitaker Institute of Biomedical Engineering (S.C.), University of California–San Diego, La Jolla, Calif.
Correspondence to John Y.-J. Shyy, PhD, Division of Biomedical Sciences, University of California–Riverside, Riverside, CA 92521-0121. E-mail john.shyy{at}ucr.edu
The focal pattern of atherosclerotic lesions in arterial vessels suggests that local blood flow patterns are important factors in atherosclerosis. Although disturbed flows in the branches and curved regions are proatherogenic, laminar flows in the straight parts are atheroprotective. Results from in vitro studies on cultured vascular endothelial cells with the use of flow channels suggest that integrins and the associated RhoA small GTPase play important roles in the mechanotransduction mechanism by which shear stress is converted to cascades of molecular signaling to modulate gene expression. By interacting dynamically with extracellular matrix proteins, the mechanosensitive integrins activate RhoA and many signaling molecules in the focal adhesions and cytoplasm. Through such mechanotransduction mechanisms, laminar shear stress upregulates genes involved in antiapoptosis, cell cycle arrest, morphological remodeling, and NO production, thus contributing to the atheroprotective effects. This review summarizes some of the recent findings relevant to these mechanotransduction mechanisms. These studies show that integrins play an important role in mechanosensing in addition to their involvement in cell attachment and migration.
Key Words: shear stress • mechanotransduction • endothelium • integrins • Rho
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