Journal
NATURE MEDICINE
Volume 7, Issue 6, Pages 699-705Publisher
NATURE AMERICA INC
DOI: 10.1038/89076
Keywords
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Funding
- NHLBI NIH HHS [R01 HL065405, HL65405-01, F32 HL075970] Funding Source: Medline
- NIDDK NIH HHS [T32 DK7061, T32 DK007061] Funding Source: Medline
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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.
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