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1 Department of Pharmacology, College of Medicine, University of South Alabama, Mobile, Alabama 36688; 2 Johns Hopkins Asthma and Allergy Center, Department of Pulmonary and Critical Care, Baltimore, Maryland 21224; 3 Pulmonary Division, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52242; 4 Department of Medicine, Columbia University, New York, New York 10019; and 5 Department of Pharmacology, College of Medicine, University of Illinois-Chicago, Chicago, Illinois 60612
Endothelium forms a physical barrier that separates blood from tissue. Communication between blood and tissue occurs through the delivery of molecules and circulating substances across the endothelial barrier by directed transport either through or between cells. Inflammation promotes macromolecular transport by decreasing cell-cell and cell-matrix adhesion and increasing centripetally directed tension, resulting in the formation of intercellular gaps. Inflammation may also increase the selected transport of macromolecules through cells. Significant progress has been made in understanding the molecular and cellular mechanisms that account for constitutive endothelial cell barrier function and also the mechanisms activated during inflammation that reduce barrier function. Current concepts of mechanisms regulating endothelial cell barrier function were presented in a symposium at the 2000 Experimental Biology Conference and are reviewed here.
gp60; myosin light chain kinase; vascular endothelial-cadherin; adenyl cyclase; calcium
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