Reciprocal Regulation of Endothelial Substrate Adhesion and Barrier Function

• DOI: 10.1111/j.1549-8719.2001.tb00186.x
• Publication Date: 2010-01-26T10:26:14Z
• Authors: J. STEVEN ALEXANDER; YANAN ZHU; JOHN W. ELROD; BRETT ALEXANDER; LAURA COE; T.J. KALOGERIS; JOHN FUSELER
• Keywords: Barrier function; Paxillin; Vinculin

ABSTRACT Objective : To examine how cell‐substrate adhesion is regulated during barrier changes produced by exposure to inflammatory mediators. Methods Lung microvascular endothelial monolayers were treated with test agents ± blockers, and was measured transendothelial resistance; assessed surface area conservation after trypsin treatment of monolayers. Protein phosphorylation distribution assayed immunoblotting fluorescent microscopy, respectively. Results H 2 O , histamine, bradykinin, thrombin, decreased function, enhanced the substratum. cell substrate in a concentration (0–1 mM)‐ time (0–60 minutes)‐ dependent fashion. This effect reversed within 120 minutes removal blocked mean arterial pressure (MAP) kinase inhibitor, PD98059 chelating cytoplasmic Ca 2+ but not PKC or PKG inhibition. also stimulated tyrosine several proteins increased association focal adhesive paxillin, talin, vinculin cytoskeleton may promote localization these junctions. Conclusions Our data indicate that mediators reduce cell‐cell contact, contributing reduced solute simultaneously binding, which be reciprocal events regulation vitro vivo .