Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 177, Issue 2, Pages 998-1003Publisher
ELSEVIER SCIENCE INC
DOI: 10.2353/ajpath.2010.091287
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Funding
- National Institutes of Health [R01 HL64793, R01 HL61371, R01 HL081190, P01 HL70295]
- American Heart Association
- Instituto de Salud Carlos III, Spain
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Caveolin-1 (Cav-1) is the major structural protein essential to the formation of the caveolae in endothelial cells. Genetic ablation of Cav-1 on an apolipoprotein E knockout background inhibits the progression of atherosclerosis, whereas re-expression of Cav-1 in the endothelium promotes lesion expansion. Although Cav-1-null mice are useful to delineate the importance of caveolae in atherosclerosis, there are additional problems that are difficult to dissect because loss of Cav-1 abolishes both the caveolae organelle as well as the Cav-1-mediated signaling pathways. To study how Cav-1 influences the progression of atherosclerosis in mice with caveolae, we generated a transgenic mouse that overexpresses Cav-1 in the endothelial cells in an apolipoprotein E-deficient background. We found that endothelial-specific overexpression of Cav-1 enhanced the progression of atherosclerosis in mice. Mechanistically, overexpression of Cav-1 reduced endothelial cell proliferation, migration, and nitric oxide production in vitro and increased expression of vascular cell adhesion molecule-1 in vivo. (Am J Pathol 2010,177:998-1003; DOI: 10.2353/ajpath.2010.091287)
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