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The FASEB Journal, Vol 9, 910-918, Copyright © 1995 by The Federation of American Societies for Experimental Biology
REVIEWS |
E Dejana, M Corada and MG Lampugnani
CEA, Laboratories of Hematologie, INSERM U217, Departement de Biologie Moleculaire et Structurale, CEN-Grenoble, France.
The endothelium forms the main barrier to the passage of macromolecules and circulating cells from blood to tissues. Endothelial permeability is in large part regulated by intercellular junctions. These are complex structures formed by transmembrane adhesive molecules linked to a network of cytoplasmic/cytoskeletal proteins. At least four different types of endothelial junctions have been described: tight junctions, gap junctions, adherence junctions and syndesmos. These organelles have some features and components in common with epithelial cells but there are also some that are specific for the endothelium. The mechanisms that regulate the opening and closing of endothelial junctions are still obscure. It is conceivable that inflammatory agents increase permeability by binding to specific receptors generating intracellular signals, which in turn cause cytoskeletal reorganization and opening of interendothelial cell gaps. Endothelial junctions also control leukocyte extravasation. Once leukocytes have adhered to the endothelium, a coordinated opening of interendothelial cell junctions occurs. The mechanism by which this takes place is unknown, but it might present characteristics similar to that triggered by soluble mediators.
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