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To investigate the functions of MLCK in endothelial cells <jats:italic>in\u2003vivo<\/jats:italic>, we generated a mouse model in which MLCK was selectively deleted by crossing <jats:italic>Mylk1<\/jats:italic> floxed mice with <jats:italic>Tie2\/cre<\/jats:italic> transgenic mice. Knocking out <jats:italic>Mylk1<\/jats:italic> from endothelial cells had no effect on the global phenotype of the mice, including body weight and blood pressure. Lipopolysaccharide (LPS)\u2010mediated septic death was also not altered in the knockout (KO) mice. Consistently, LPS\u2010induced inflammatory injury and the increase in microvascular permeability in the main organs, including the lung and the kidney, was not significantly attenuated in KO mice as compared with wild\u2010type mice. However, the LPS\u2010induced microvascular hyperpermeability of the esophagus and the eyeballs was attenuated in KO mice. We also found that the LPS\u2010mediated increase in the number of caveolae in the endothelial cells of the esophagus was significantly reduced in KO mice. Our results do not support a role for endothelial cell MLCK in the pathogenesis of inflammatory diseases.<\/jats:p>","DOI":"10.1111\/j.1742-4658.2012.08541.x","type":"journal-article","created":{"date-parts":[[2012,2,21]],"date-time":"2012-02-21T17:29:47Z","timestamp":1329845387000},"page":"1485-1494","source":"Crossref","is-referenced-by-count":16,"title":["Deletion of myosin light chain kinase in endothelial cells has a minor effect on the lipopolysaccharide\u2010induced increase in microvascular endothelium permeability in 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