Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-5-31
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E, http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol Esters, http://linkedlifedata.com/resource/pubmed/chemical/FABP7 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Fabp5 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Fabp7 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acid-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Glucose, http://linkedlifedata.com/resource/pubmed/chemical/Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6, http://linkedlifedata.com/resource/pubmed/chemical/Lipids, http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1078-8956
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
699-705
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11385507-Adipocytes, pubmed-meshheading:11385507-Animals, pubmed-meshheading:11385507-Aorta, pubmed-meshheading:11385507-Apolipoproteins E, pubmed-meshheading:11385507-Arteriosclerosis, pubmed-meshheading:11385507-Bone Marrow Transplantation, pubmed-meshheading:11385507-Carrier Proteins, pubmed-meshheading:11385507-Cell Line, pubmed-meshheading:11385507-Cholesterol Esters, pubmed-meshheading:11385507-Diet, pubmed-meshheading:11385507-Fatty Acid-Binding Proteins, pubmed-meshheading:11385507-Female, pubmed-meshheading:11385507-Foam Cells, pubmed-meshheading:11385507-Glucose, pubmed-meshheading:11385507-Humans, pubmed-meshheading:11385507-Insulin, pubmed-meshheading:11385507-Interleukin-1, pubmed-meshheading:11385507-Interleukin-6, pubmed-meshheading:11385507-Lipids, pubmed-meshheading:11385507-Macrophages, pubmed-meshheading:11385507-Male, pubmed-meshheading:11385507-Mice, pubmed-meshheading:11385507-Mice, Inbred C57BL, pubmed-meshheading:11385507-Mice, Transgenic, pubmed-meshheading:11385507-Neoplasm Proteins, pubmed-meshheading:11385507-Nerve Tissue Proteins, pubmed-meshheading:11385507-Tumor Necrosis Factor-alpha, pubmed-meshheading:11385507-Tumor Suppressor Proteins
pubmed:year
2001
pubmed:articleTitle
Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis.
pubmed:affiliation
Division of Biological Sciences and Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't