Nonmuscle myosin light-chain kinase deficiency attenuates atherosclerosis in apolipoprotein E-deficient mice via reduced endothelial barrier dysfunction and monocyte migration.

ABSTRACT:

Background

Endothelial dysfunction and monocyte migration are key events in the pathogenesis of atherosclerosis. Nonmuscle myosin light-chain kinase (nmMLCK), the predominant MLCK isoform in endothelial cells, has been shown to contribute to vascular inflammation by altering endothelial barrier function. However, its impact on atherogenesis remains unknown.

Methods and results

We investigated the role of nmMLCK in the development of atherosclerotic lesions in apolipoprotein E-deficient (apoE(-/-)) mice fed an atherogenic diet for 12 weeks. Histopathological examination demonstrated that nmMLCK deficiency (apoE(-/-)nmmlck(-/-)) reduced the size of aortic lesions by 53%, lipid contents by 44%, and macrophage deposition by 40%. Western blotting and reverse-transcription polymer

SUBMITTER: Sun C 

PROVIDER: S-EPMC3136817 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature