Source:http://linkedlifedata.com/resource/pubmed/id/10811597
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
19
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pubmed:dateCreated |
2000-6-16
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pubmed:abstractText |
BACKGROUND: Adhesive interactions between leukocytes and endothelial cells are characteristic of the development of atherosclerotic lesions, but the receptors involved remain to be defined. P-selectin is an adhesion receptor expressed on activated endothelial cells or platelets and was shown to be involved in fatty streak formation in LDL receptor-deficient mice on an atherogenic diet. The main purpose of this study is to examine the role of P-selectin in the spontaneous development of advanced atherosclerosis in apoE-deficient mice. METHODDS AND RESULTS: We intercrossed P-selectin-deficient mice with mice lacking apoE and compared lesion development in apoE-deficient mice with P-selectin (apoE(-/-) P(+/+)) and without P-selectin (apoE(-/-) P(-/-)) that were fed normal mouse chow. At 4 months of age, apoE(-/-) P(-/-) mice had 3. 5-fold smaller aortic sinus lesions than apoE(-/-) P(+/+) mice. These were limited to fatty streaks in the apoE(-/-) P(-/-) mice, whereas 70% of apoE(-/-) P(+/+) lesions contained smooth muscle cells. Significantly more of the aortic sinus circumference was covered by lesions in the apoE(-/-) P(+/+) animals. The P-selectin genotype affected macrophage recruitment, because twice as many mononuclear cells were present in the P-selectin-positive lesions. At 15 months, the lesions progressed to the fibrous plaque stage in both genotypes and spread throughout the aorta, but this process was delayed in apoE(-/-) P(-/-) mice. In the aortic sinus, the lesions of the apoE(-/-) P(-/-) mice were 2.6-fold smaller and less calcified. CONCLUSIONS: P-selectin appears to be a key adhesion receptor mediating leukocyte recruitment into lesions and promoting advanced atherosclerosis in apoE-deficient mice.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1524-4539
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
16
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pubmed:volume |
101
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2290-5
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10811597-Animals,
pubmed-meshheading:10811597-Aorta,
pubmed-meshheading:10811597-Apolipoproteins E,
pubmed-meshheading:10811597-Arteriosclerosis,
pubmed-meshheading:10811597-Disease Progression,
pubmed-meshheading:10811597-Mice,
pubmed-meshheading:10811597-Mice, Inbred C57BL,
pubmed-meshheading:10811597-Monocytes,
pubmed-meshheading:10811597-P-Selectin,
pubmed-meshheading:10811597-Sinus of Valsalva,
pubmed-meshheading:10811597-Time Factors
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pubmed:year |
2000
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pubmed:articleTitle |
Prominent role of P-selectin in the development of advanced atherosclerosis in ApoE-deficient mice.
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pubmed:affiliation |
Center for Blood Research, Department of Pathology, Harvard Medical School, Boston, Massachusetts, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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