Abstract
The function of cytoskeletal proteins in the modulation of vascular smooth muscle cell (SMC) phenotype during vascular disease is poorly understood. In this report, we used a combination of gene targeting and Cre/lox-mediated cell fate mapping in mice to investigate the role of SM22alpha, an SMC-specific cytoskeletal protein of unknown function, in the development of atherosclerosis. In hypercholesterolemic ApoE-deficient mice, genetic ablation of SM22alpha resulted in increased atherosclerotic lesion area and a higher proportion of proliferating SMC-derived plaque cells. These results identify a role for SM22alpha in the regulation of SMC phenotype during atherogenesis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aortic Diseases / genetics
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Aortic Diseases / metabolism
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Aortic Diseases / pathology
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Apolipoproteins E / deficiency
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Apolipoproteins E / genetics
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Arteriosclerosis / genetics
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Arteriosclerosis / metabolism*
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Arteriosclerosis / pathology
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Cell Division
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Cell Lineage
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Genes, Reporter
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Hyperlipoproteinemia Type II / genetics
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Hyperlipoproteinemia Type II / metabolism
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Mice
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Mice, Knockout
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Microfilament Proteins / deficiency
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Microfilament Proteins / genetics
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Microfilament Proteins / physiology*
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Muscle Proteins / deficiency
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Muscle Proteins / genetics
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Muscle Proteins / physiology*
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Muscle, Smooth, Vascular / metabolism
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Muscle, Smooth, Vascular / pathology*
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Myocytes, Smooth Muscle / metabolism
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Myocytes, Smooth Muscle / ultrastructure*
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Phenotype
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Recombination, Genetic
Substances
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Apolipoproteins E
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Microfilament Proteins
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Muscle Proteins
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Tagln protein, mouse
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transgelin