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  • Title: Inflammation-induced subcellular redistribution of VE-cadherin, actin, and gamma-catenin in cultured human lung microvessel endothelial cells.
    Author: Lim MJ, Chiang ET, Hechtman HB, Shepro D.
    Journal: Microvasc Res; 2001 Nov; 62(3):366-82. PubMed ID: 11678639.
    Abstract:
    The inflammation-induced subcellular redistribution of key cytoskeletal and junctional proteins in cultured human lung microvessel endothelial cells is investigated as part of a study on the posttranslational regulation of paracellular permeability. Inflammatory agonist-stimulated cells are detergent fractionated into three subcellular compartments followed by quantitative immunoblot analysis. Actin, gamma-catenin, and VE-cadherin increasingly associate with the cytoskeletal fraction upon thrombin stimulation. Concomitantly, actin is reduced in the cytosol fraction, whereas gamma-catenin and VE-cadherin are reduced in the membrane fraction. alpha- and beta-catenin show baseline distributions similar to those of VE-cadherin and gamma-catenin, but do not significantly redistribute. Additionally, vimentin is found exclusively in the cytoskeletal fraction and also does not significantly redistribute following thrombin treatment. The VE-cadherin response is independent of the presence of F-actin or actin redistribution. Immunofluorescence microscopy reveals that membrane and cytoskeletal VE-cadherin is present in alternating patches along the cell junctions. Furthermore, VE-cadherin is lost from zones of interendothelial cell pore formation. A model is formulated describing these membrane-associated VE-cadherin patches as predetermined zones of potential intercellular gap formation. During inflammation, VE-cadherin is lost from these zones and sequestered at the remaining cell-cell contact sites, anchored to the cytoskeleton in an actin-independent fashion.
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