Send to

Choose Destination
Nat Med. 2001 Jun;7(6):699-705. doi: 10.1038/89076.

Lack of macrophage fatty-acid-binding protein aP2 protects mice deficient in apolipoprotein E against atherosclerosis.

Author information

Division of Biological Sciences and Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA.
Departments of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Bristol-Myers Squibb PRI, Department of Metabolic Research, Princeton, New Jersey, USA.
Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky, USA.
Pathology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Contributed equally


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.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center