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Brief Review |
From the Max-Planck-Institute of Molecular Biomedicine, Münster, Germany.
Correspondence to Dr Dietmar Vestweber, Max-Planck-Institute of Molecular Biomedicine, Röntgenstr. 20, D-48149 Münster, Germany. E-mail vestweb{at}mpi-muenster.mpg.de
Series Editor: Dietmar Vestweber
Vascular Adhesion Molecules
ATVB In Focus
Previous Brief Reviews in this Series:
van Buul JD, Kanters E, Hordijk PL. Endothelial signaling by Ig-like cell adhesion molecules. Arterioscler Thromb Vasc Biol. 2007;27:1870–1876.
Bradfield PF, Nourshargh S, Aurrand-Lions M, Imhof BA. JAM family and related proteins in leukocyte migration. Arterioscler Thromb Vasc Biol. 2007;27:2104–2112.
Galkina E and Ley K. Vascular adhesion molecules in atherosclerosis. Arterioscler Thromb Vasc Biol. 2007;27: 2292–2301.
Jalkanen S, Salmi M. VAP-1 and CD73, endothelial cell surface enzymes in leukocyte extravasation. Arterioscler Thromb Vasc Biol. 2008;28:18–26.
Vascular endothelial (VE)-cadherin is a strictly endothelial specific adhesion molecule located at junctions between endothelial cells. In analogy of the role of E-cadherin as major determinant for epithelial cell contact integrity, VE-cadherin is of vital importance for the maintenance and control of endothelial cell contacts. Mechanisms that regulate VE-cadherin–mediated adhesion are important for the control of vascular permeability and leukocyte extravasation. In addition to its adhesive functions, VE-cadherin regulates various cellular processes such as cell proliferation and apoptosis and modulates vascular endothelial growth factor receptor functions. Consequently, VE-cadherin is essential during embryonic angiogenesis. This review will focus on recent new developments in understanding the role of VE-cadherin in controlling endothelial cell contacts and influencing endothelial cell behavior by various outside-in signaling processes.
Key Words: vascular permeability VE-cadherin leukocyte extravasation cell adhesion
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