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Prevalent proposals suggest that myosin light chain kinase (MLCK) plays a critical role in endothelial permeability.To determine the function of MLCK in endothelial cells in vivo, we generated a mouse model with specific deletion of total MLCK (long and short) in endothelial cells.The knock out mice displayed normal appearance, growth, life span and physiological phenotypes.Morphology of the mutant endothelial cells appears normal also.To evaluate MLCK function in endothelial permeability, we examined the effect of Lipopolysaeeharide (LPS) on MLCK-deficient mice.