Microvascular permeability and barrier function are dependent on maintenance of tight cell-cell intercellular junctions. Adjacent cells assemble junctions composed of transmembrane proteins linked to cytoplasmic multiprotein plaques that anchor microfilament or IF cytoskeletal networks to the plasma membrane. Microvascular EC junctional adhesive plaques maintain cell morphology, tissue integrity, and a semipermeable barrier and participate in cell signaling pathways. Endothelial cells contain microfilament-associated adherens junctions and tight junctions. Vascular endothelial cadherin (VE-cad) is an important component of the Ca2+-dependent EC adherens junction and, along with other junctional proteins such as desmoplakin and p- and g-catenin (plakoglobin), link the actin and vimentin intermediate filament networks of adjacent cells.
Inflammatory factors affect vascular permeability by disturbing cell-cell junctions and the vimentin IF network. His-tamine decreases EC barrier function, most likely by rapidly increasing phosphorylation of multiple junctional proteins including VE-cadherin and vimentin and inducing a rapid reorganization of the vimentin IF. Biochemical studies reveal that the histamine treatment decreases association between the vimentin cytoskeleton and VE-cadherin, but not actin and VE-cadherin . The IF network may then participate structurally and also appears to be involved in assembly and function of microvascular endothelial cell-substrate and cell-cell attachment that effects endothelial cell function.
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