Abstract
Interendothelial junctions in continuous endothelium are the primary pathway for the passage of fluid, solutes, and leukocytes from the intravascular compartment to the interstitium. The maintenance of these channels is in part a function of circulating metabolites and local secretions produced by the cells of the microvessel wall. When this regulatory mechanism is disrupted, such as in an acute inflammatory response, interendothelial gaps appear and the microvascular barrier is compromised. Glycosylated cell surface proteins are believed to play a role in the development and maintenance of junctional apposition, and hence permeability. A predictable response of microvascular endothelial cells to an inflammatory stimulus therefore should be a change in junction-associated glycoproteins. Moreover, the heterogeneity of microvascular endothelial barrier properties may in part be a function of specific glycans involved in cell-cell contact. To test these suppositions, the binding of a panel of lectins to cult...
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