Mechanisms of increased endothelial permeability

Canadian Journal of Physiology and Pharmacology
H Lum, A B Malik

Abstract

The increase in endothelial permeability in response to inflammatory mediators such as thrombin and histamine is accompanied by reversible cell rounding and interendothelial gap formation, suggesting that the predominant transport pathway is a diffusive one (i.e., via cellular junctions (paracellular transport)). However, vesicle-mediated transport (i.e., via albumin-binding protein gp60) may also contribute significantly to the overall increase in permeability. Regulation of paracellular transport in endothelial cells is associated with modulation of actin-based systems, which anchor the cell to its neighbor or extracellular matrix, thus maintaining endothelial integrity. At the cell-cell junctions, actin is linked indirectly to the plasma membrane by linking proteins (e.g., vinculin, catenins, alpha-actinin) to cadherins, which function in homophilic intercellular adhesion. At endothelial focal contacts, the transmembrane receptors (integrins) for matrix proteins are linked to actin via linking proteins (i.e., vinculin, talin, alpha-actinin). In response to inflammatory mediators, second messengers signal two regulatory pathways, which modulate the actin-based systems, and can thus lead to impairment of the endothelial barrie...Continue Reading

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