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Journal of Cell Science, Vol 110, Issue 5 583-588, Copyright © 1997 by Company of Biologists
JOURNAL ARTICLES |
U Gotsch, E Borges, R Bosse, E Boggemeyer, M Simon, H Mossmann and D Vestweber
Institute of Cell Biology, ZMBE, University of Munster, Germany.
Neutrophils enter sites of inflammation by crossing the endothelial lining of the blood vessel wall. VE-cadherin is an endothelial specific, homophilic adhesion molecule located at the lateral cell surface. We have generated a monoclonal antibody against mouse VE-cadherin which inhibits electrical resistance of endothelial cell monolayers in vitro as well as aggregation of VE-cadherin transfected cells. In vivo, this antibody was found to increase vascular permeability and to accelerate the entry of neutrophils into chemically inflamed mouse peritoneum. Thus, VE-cadherin is essential for the integrity of the endothelial barrier in vivo. Our data suggest that opening of VE-cadherin mediated endothelial cell contacts may be a relevant step during neutrophil extravasation.
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