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Deletion of myosin light chain kinase in endothelial cells has a minor effect on the lipopolysaccharide‐induced increase in microvascular endothelium permeability in mice

AbstractPrevalent proposals suggest that myosin light chain kinase (MLCK) plays a critical role in endothelial permeability. To investigate the functions of MLCK in endothelial cells (ECs) in vivo, we generated a mouse model in which MLCK was selectively deleted by crossing Mylk1 floxed mice with Tie2‐cre transgenic mice. Knocking out the Mylk1 gene from ECs has no effect on the global phenotype of the mice, including body weight and blood pressure. Lipopolysaccharide (LPS)‐mediated septic death was not altered in the knockout (KO) mice either. Consistently, the LPS‐induced inflammatory injury and...

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Published By: MedWorm/DeathRecovery - Wednesday, 22 February

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