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- ISSN
- 1079-5642
- eISSN
- 1524-4636
- DOI
- 10.1161/01.ATV.0000237629.29842.4c
- pmid
- 16857950
- Publisher site
- See Article on Publisher Site
Abstract
Atherosclerosis and Lipoproteins Macrophage ABCG1 Deletion Disrupts Lipid Homeostasis in Alveolar Macrophages and Moderately Influences Atherosclerotic Lesion Development in LDL Receptor-Deficient Mice Ruud Out, Menno Hoekstra, Reeni B. Hildebrand, Janine K. Kruit, Illiana Meurs, Zhaosha Li, Folkert Kuipers, Theo J.C. Van Berkel, Miranda Van Eck Objective—ABCG1 has recently been identified as a facilitator of cellular cholesterol and phospholipid efflux to high-density lipoprotein (HDL). Its expression in macrophages is induced during cholesterol uptake in macrophages and by liver X receptor (LXR). The role of macrophage ABCG1 in atherosclerotic lesion development is, however, still unknown. Methods and Results—To assess the role of macrophage ABCG1 in atherosclerosis, we generated low-density lipoprotein (LDL) receptor knockout (LDLr ) mice that are selectively deficient in macrophage ABCG1 by using bone marrow / / / transfer (ABCG1 3 LDLr ). Peritoneal macrophages isolated from donor ABCG1 mice exhibited a 22% (P0.0007) decrease in cholesterol efflux to HDL. To induce atherosclerosis, transplanted mice were fed a high-cholesterol diet containing 0.25% cholesterol and 15% fat for 6 and 12 weeks. Serum lipid levels and lipoprotein / / / profiles did not differ significantly between ABCG1 3 LDLr mice and controls. In lungs of ABCG1 3 LDLr mice a
Journal
Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health
Published: Oct 1, 2006