Source:http://linkedlifedata.com/resource/pubmed/id/20382259
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
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| pubmed:dateCreated |
2010-5-31
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| pubmed:abstractText |
Caveolae and its structural protein caveolin-1 (Cav-1) are abundant in vascular endothelial cells (ECs). We examined whether caveolae are involved in monocyte adhesion to ECs responding to a synergy of hypercholesterolemia and inflammation. Treating human umbilical vein ECs with cholesterol enhanced endotoxin lipopolysaccharide (LPS)-induced monocyte adhesion. Use of isolated caveolae-enriched membranes revealed that cell adhesion molecules (CAMs), including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), co-localized with Cav-1 in caveolae. LPS upregulated CAMs expression and increased the co-localization. Cholesterol exposure decreased the level of CAMs in the caveolae. Co-immunoprecipitation and confocal microscopy revealed that ICAM-1 interacted with Cav-1. Electron microscopy showed that ICAM-1 was mainly located in caveolae. Cholesterol exposure decreased this interaction and drove ICAM-1 out of caveolae. Knockdown of Cav-1 reduced the synergistic effects of cholesterol and inflammation. In vivo, ICAM-1 and Cav-1 co-localization was lower in the aortic endothelium of ApoE(-)(/)(-) mice than in that of wild-type controls. Cav-1 negatively regulates monocyte adhesion by the co-localization of CAMs in caveolae, which is disturbed by cholesterol. Thus, our study suggests a molecular basis underlying the synergistic effects of hypercholesterolemia and inflammation in atherogenesis.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E,
http://linkedlifedata.com/resource/pubmed/chemical/Caveolin 1,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0006-3002
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2010 Elsevier B.V. All rights reserved.
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| pubmed:issnType |
Print
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| pubmed:volume |
1801
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
702-10
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| pubmed:meshHeading |
pubmed-meshheading:20382259-Animals,
pubmed-meshheading:20382259-Apolipoproteins E,
pubmed-meshheading:20382259-Biological Transport,
pubmed-meshheading:20382259-Cattle,
pubmed-meshheading:20382259-Caveolae,
pubmed-meshheading:20382259-Caveolin 1,
pubmed-meshheading:20382259-Cell Adhesion,
pubmed-meshheading:20382259-Cholesterol,
pubmed-meshheading:20382259-Endothelium, Vascular,
pubmed-meshheading:20382259-Gene Expression Regulation,
pubmed-meshheading:20382259-Humans,
pubmed-meshheading:20382259-Hypercholesterolemia,
pubmed-meshheading:20382259-Inflammation,
pubmed-meshheading:20382259-Intercellular Adhesion Molecule-1,
pubmed-meshheading:20382259-Lipopolysaccharides,
pubmed-meshheading:20382259-Mice,
pubmed-meshheading:20382259-Mice, Knockout,
pubmed-meshheading:20382259-Monocytes,
pubmed-meshheading:20382259-Vascular Cell Adhesion Molecule-1
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| pubmed:year |
2010
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| pubmed:articleTitle |
Cholesterol increases adhesion of monocytes to endothelium by moving adhesion molecules out of caveolae.
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| pubmed:affiliation |
Department of Physiology and Pathophysiology, Key Laboratory of Molecular Cardiovascular Sciences of Education Ministry, Peking University Health Science Center, Beijing 100091, China.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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