Skip to content Skip to navigation

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

余洋 吕宁 陆峥 郑艳艳 张文呈陈晨彭亚静 何伟奇 朱敏生 陈华群

There is a current view that myosin light chain kinase (MLCK) plays a critical role in endothelial permeability. To investigate the functions of MLCK in endothelial cells 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 Mylk1 from endothelial cells had no effect on the global phenotype of the mice, including body weight and blood pressure. Lipopolysaccharide (LPS)-mediated septic death was also not altered in the knockout (KO) mice. Consistently, LPS-induced 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-type mice. However, the LPS-induced microvascular hyperpermeability of the esophagus and the eyeballs was attenuated in KO mice. We also found that the LPS-mediated 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. Introduction The vascular endothelium forms a semipermeable barrier between the bloodstream and interstitial space [1,2]. The intact endothelial barrier is restrictive to cells, proteins, fluid, and solutes, thus maintaining vascular homeostasis and the physiological functions of different organs [3]. In the development of a variety of inflammatory diseases, such