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Circulation Research. 1999;84:315-322

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(Circulation Research. 1999;84:315-322.)
© 1999 American Heart Association, Inc.


Original Contribution

Exposure of Human Vascular Endothelial Cells to Sustained Hydrostatic Pressure Stimulates Proliferation

Involvement of the {alpha}V Integrins

Eric A. Schwartz, Rena Bizios, Marvin S. Medow, Mary E. Gerritsen

From the Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY (E.A.S., R.B.); the Department of Pediatrics, New York Medical College, Valhalla, NY (M.S.M.); and the Department of Cardiovascular Research, Genentech, Inc, South San Francisco, Calif (M.E.G.).

Abstract—The present study investigated the effects of sustained hydrostatic pressure (SHP; up to 4 cm H2O) on human umbilical vein endothelial cell (HUVEC) proliferation, focal adhesion plaque (FAP) organization, and integrin expression. Exposure of HUVECs to SHP stimulated cell proliferation and a selective increase in the expression of integrin subunit {alpha}V. The increase in {alpha}V was observed as early as 4 hours after exposure to pressure and preceded detectable increases in the bromodeoxyuridine labeling index. Laser confocal microscopy studies demonstrated colocalization of the {alpha}V integrin to FAPs. The individual FAPs in pressure-treated cells demonstrated a reduced area and increased aspect ratio and were localized to both peripheral and more central regions of the cells, in contrast to the predilection for the cell periphery in cells maintained under control pressure conditions. The pressure-induced changes in {alpha}V distribution had functional consequences on the cells: adhesivity of the cells to vitronectin was increased, and {alpha}V antagonists blocked the pressure-induced proliferative response. Thus, the present study suggests a role for {alpha}V integrins in the mechanotransduction of pressure by endothelial cells.


Key Words: mechanotransduction • hydrostatic pressure • integrin • human umbilical vein endothelial cell • cell proliferation




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