作者: M. Corada , M. Mariotti , G. Thurston , K. Smith , R. Kunkel
关键词: Adherens junction 、 Cingulin 、 Biology 、 Cell junction 、 Endothelium 、 Platelet Endothelial Cell Adhesion Molecule 、 Vascular permeability 、 Cadherin 、 Tight junction 、 Cell biology
摘要: In the present paper, we characterize an antibody, mAb BV13, directed to mouse vascular endothelial (VE)-cadherin, a major adhesive protein of interendothelial adherens junctions. When added cultured cells, BV13 induces redistribution VE-cadherin from intercellular did not change localization platelet cell adhesion molecule or tight junction markers such as zonula occludens 1, cingulin, and junctional molecule. Intravenous administration induced concentration- time-dependent increase in permeability heart lungs. By electron microscopy, interstitial edema accumulation mixed types inflammatory cells lungs were observed. Injection (rhodamine-labeled) Ricinus communis I lectin showed focal spots exposed basement membrane alveolar capillaries some larger pulmonary vessels. These data indicate that is required for integrity normal organ functions.