Source:http://linkedlifedata.com/resource/pubmed/id/19065319
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5-6
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pubmed:dateCreated |
2008-12-9
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pubmed:abstractText |
Previous studies showed that p66(Shc-/-) mice on a very-high-fat diet (HFD) had reduced oxidative stress, foam cell, and early atherosclerotic lesion formation. Here, the authors have used hypercholesterolemic apolipoprotein E (ApoE(-/-)) mice to investigate the role of p66Shc deletion in advanced atheroma. The authors generated mice deficient of both ApoE and p66Shc genes (ApoE(-/-) /p66(Shc-/-)). They used microsatellite polymerase chain reaction (PCR) analysis to analyze the genetic background and considered only animals with a constant percentages of C57B6L and 129SV background strands (it was obtained the 50.3% +/- 6.4% of C57B6L background). Computer-assisted analysis revealed that advanced atherosclerotic lesions in ApoE(-/-)/p66(Shc+/+) were significantly larger than those observed in ApoE(-/-)/p66(Shc-/-). Accordingly, the lipid-laden macrophage foam cells and oxidation-specific epitopes in ApoE(-/-)/p66(shc+/+) HFD-treated groups were higher than those observed in normal diet (ND)-treated groups. Thus, p66(Shc-/-) plays an important protective role also against advanced atherosclerotic lesion formation. Finally, the authors have used microarray to investigate major changes in gene expression in aortas of mice with ApoE(-/-)/p66(Shc-/-) background treated with a very HFD in comparison to ApoE(-/-)/p66(Shc+/+) (these data have been confirmed by by real-time PCR and immunohistochemistry). DAVID (Database for Annotation, Visualization and Integrated Discovery) analysis revealed that CD36 antigen (CD36), tissue inhibitor of metalloproteinase 2 (TIMP2), apolipoprotein E (ApoE), acetyl-coenzyme A acetyltransferase 1 (ACAT1), and thrombospondin 1 (THBS1) can be involved in p66 deletion-dependent vascular protection through the adipocytokine/lipid signaling pathway.
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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/Adipokines,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E,
http://linkedlifedata.com/resource/pubmed/chemical/Dietary Fats,
http://linkedlifedata.com/resource/pubmed/chemical/Shc Signaling Adaptor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Shc1 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:issn |
1029-2373
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pubmed:author |
pubmed-author:De RosaGaetanoG,
pubmed-author:GiorgioMarcoM,
pubmed-author:LermanLilach OLO,
pubmed-author:MansuetoGelsominaG,
pubmed-author:Martin-PaduraInesI,
pubmed-author:MigliaccioEnricaE,
pubmed-author:MinardiSimoneS,
pubmed-author:NapoliClaudioC,
pubmed-author:PelicciPier GiuseppePG,
pubmed-author:RienzoMonicaM,
pubmed-author:StendardoMassimoM,
pubmed-author:de NigrisFilomenaF
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pubmed:issnType |
Electronic
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
276-87
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pubmed:meshHeading |
pubmed-meshheading:19065319-Adipokines,
pubmed-meshheading:19065319-Animals,
pubmed-meshheading:19065319-Aorta,
pubmed-meshheading:19065319-Apolipoproteins E,
pubmed-meshheading:19065319-Atherosclerosis,
pubmed-meshheading:19065319-Dietary Fats,
pubmed-meshheading:19065319-Disease Models, Animal,
pubmed-meshheading:19065319-Down-Regulation,
pubmed-meshheading:19065319-Foam Cells,
pubmed-meshheading:19065319-Food, Formulated,
pubmed-meshheading:19065319-Gene Deletion,
pubmed-meshheading:19065319-Gene Expression Regulation,
pubmed-meshheading:19065319-Genetic Predisposition to Disease,
pubmed-meshheading:19065319-Genotype,
pubmed-meshheading:19065319-Hypercholesterolemia,
pubmed-meshheading:19065319-Lipid Metabolism,
pubmed-meshheading:19065319-Male,
pubmed-meshheading:19065319-Mice,
pubmed-meshheading:19065319-Mice, Inbred C57BL,
pubmed-meshheading:19065319-Mice, Knockout,
pubmed-meshheading:19065319-Shc Signaling Adaptor Proteins,
pubmed-meshheading:19065319-Signal Transduction
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pubmed:articleTitle |
p66Shc deletion confers vascular protection in advanced atherosclerosis in hypercholesterolemic apolipoprotein E knockout mice.
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pubmed:affiliation |
European Institute of Oncology (EIO), Milan, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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