| pubmed-article:11385507 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C0919496 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C0968902 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C0004153 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C0003595 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C1333527 | lld:lifeskim |
| pubmed-article:11385507 | lifeskim:mentions | umls-concept:C1415350 | lld:lifeskim |
| pubmed-article:11385507 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:11385507 | pubmed:dateCreated | 2001-5-31 | lld:pubmed |
| pubmed-article:11385507 | pubmed:abstractText | The adipocyte fatty-acid-binding protein, aP2, has an important role in regulating systemic insulin resistance and lipid metabolism. Here we demonstrate that aP2 is also expressed in macrophages, has a significant role in their biological responses and contributes to the development of atherosclerosis. Apolipoprotein E (ApoE)-deficient mice also deficient for aP2 showed protection from atherosclerosis in the absence of significant differences in serum lipids or insulin sensitivity. aP2-deficient macrophages showed alterations in inflammatory cytokine production and a reduced ability to accumulate cholesterol esters when exposed to modified lipoproteins. Apoe-/- mice with Ap2+/+ adipocytes and Ap2-/- macrophages generated by bone-marrow transplantation showed a comparable reduction in atherosclerotic lesions to those with total aP2 deficiency, indicating an independent role for macrophage aP2 in atherogenesis. Through its distinct actions in adipocytes and macrophages, aP2 provides a link between features of the metabolic syndrome and could be a new therapeutic target for the prevention of atherosclerosis. | lld:pubmed |
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| pubmed-article:11385507 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11385507 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11385507 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11385507 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11385507 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11385507 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11385507 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11385507 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11385507 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11385507 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11385507 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:11385507 | pubmed:issn | 1078-8956 | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:MaedaKK | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:ParkerR ARA | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:MorganM AMA | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:BabaevV RVR | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:FazioSS | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:MakowskiLL | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:HotamisligilG... | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:LintonM FMF | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:SuttlesJJ | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:UysalK TKT | lld:pubmed |
| pubmed-article:11385507 | pubmed:author | pubmed-author:BoordJ BJB | lld:pubmed |
| pubmed-article:11385507 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11385507 | pubmed:volume | 7 | lld:pubmed |
| pubmed-article:11385507 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11385507 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11385507 | pubmed:pagination | 699-705 | lld:pubmed |
| pubmed-article:11385507 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:11385507 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11385507 | pubmed:articleTitle | Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis. | lld:pubmed |
| pubmed-article:11385507 | pubmed:affiliation | Division of Biological Sciences and Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA. | lld:pubmed |
| pubmed-article:11385507 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11385507 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11385507 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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