ArticleCirculation2011
Nonmuscle myosin light-chain kinase deficiency attenuates atherosclerosis in apolipoprotein E-deficient mice via reduced endothelial barrier dysfunction and monocyte migration.
Article in Circulation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 102 citations in OpenAlex.
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- Influenza and cardiovascular disease pathophysiology: strings attached.European heart journal supplements : journal of the European Society of Cardiology · 2023Article
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- Pathogenic role of microRNAs in atherosclerotic ischemic stroke: Implications for diagnosis and therapy.Genes & diseases · 2022Review
- Astragaloside IV alleviates atherosclerosis through targeting circ_0000231/miR-135a-5p/CLIC4 axis in AS cell model in vitro.Molecular and cellular biochemistry · 2021Article
- HDAC1 and 2 regulate endothelial VCAM-1 expression and atherogenesis by suppressing methylation of theTheranostics · 2021Article
- Sinner or Saint?: Nck Adaptor Proteins in Vascular Biology.Frontiers in cell and developmental biology · 2021Review
- Pyk2/MCU Pathway as a New Target for Reversing Atherosclerosis.Frontiers in cell and developmental biology · 2021Article
- Salidroside Ameliorated Intermittent Hypoxia-Aggravated Endothelial Barrier Disruption and AtherosclerosisFrontiers in pharmacology · 2021Article
- Noncanonical function of long myosin light chain kinase in increasing ER-PM junctions and augmentation of SOCE.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
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- IRF-1 mediates the suppressive effects of mTOR inhibition on arterial endothelium.Journal of molecular and cellular cardiology · 2020Article
- Focal adhesion kinase and Src mediate microvascular hyperpermeability caused by fibrinogen- γC- terminal fragments.PloS one · 2020Article
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- Nonmuscle Myosin Light Chain Kinase: A Key Player in Intermittent Hypoxia-Induced Vascular Alterations.Journal of the American Heart Association · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEndothelial 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
resultsWe 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 polymerase chain reaction revealed the expression of nmMLCK in aortic endothelial cells and peripheral blood monocytes. Measurements of transendothelial electric resistance indicated that nmMLCK deficiency attenuated endothelial barrier dysfunction caused by thrombin, oxidized low-density lipoprotein, and tumor necrosis factor α. In monocytes, nmMLCK deficiency reduced their migration in response to the chemokine monocyte chemoattractant protein-1. Further mechanistic studies showed that nmMLCK acted through both myosin light chain phosphorylation-coupled and -uncoupled pathways; the latter involved Rous sacracoma virus homolog genes-encoded tyrosine kinases (Src) signaling. Moreover, depletion of Src via gene silencing, site-specific mutagenesis, or pharmacological inhibition of Src greatly attenuated nmMLCK-dependent endothelial barrier dysfunction and monocyte migration.
conclusionsNonmuscle myosin light-chain kinase contributes to atherosclerosis by regulating endothelial barrier function and monocyte migration via mechanisms involving not only kinase-mediated MLC phosphorylation but also Src activation.
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