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.
VE-cadherin antibody accelerates neutrophil recruitment in vivo
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U. Gotsch, E. Borges, R. Bosse, E. Boggemeyer, M. Simon, H. Mossmann, D. Vestweber; VE-cadherin antibody accelerates neutrophil recruitment in vivo. J Cell Sci 1 March 1997; 110 (5): 583–588. doi: https://doi.org/10.1242/jcs.110.5.583
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