Endothelial Junctional Protein Internalization in Inflammation

Junctional proteins (cadherins and occludin) are important components of endothelial adherens and tight junctions that are remodeled during inflammation, potentially through transient internalization. Junctional protein displacement from the cell surface could represent an important mechanism to decrease homotypic bonding, allowing transient increases in solute flux. Later recycling of these elements to the cell surface would restore junction competence and barrier. Ca++‐switch and exposure to inflammatory mediators promote the internalization of endothelial pan‐reactive and VE‐cadherins but not occludin which redistributes, but is apparently not remodeled acutely. These internalization events are actin‐cytoskeleton and PKC‐dependent and can be correlated with simultaneous reciprocal changes in cell‐substrate adhesion which may maintain structural integrity during periods of altered microvascular barrier.