Original Contribution |
V Integrins
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.).
AbstractThe 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
V. The increase in
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
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
V distribution had functional consequences on the cells:
adhesivity of the cells to vitronectin was increased, and
V antagonists blocked the pressure-induced
proliferative response. Thus, the present study suggests a role for
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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