Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:630-637
Published online before print March 7, 2002, doi: 10.1161/01.ATV.0000014804.35824.DA
Published online before print March 7, 2002, doi: 10.1161/01.ATV.0000014804.35824.DA
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© 2002 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Increased Atherosclerosis in Hyperlipidemic Mice With Inactivation of ABCA1 in Macrophages
From Pfizer Global Research and Development, Groton, Conn
Correspondence to Robert J. Aiello or Omar L. Francone, Pfizer Global Research and Development, Department of Cardiovascular and Metabolic Diseases, Eastern Point Rd, Groton, CT 06340. E-mail Robert_J_Aiello{at}groton.pfizer.com or Omar_L_Francone@groton.pfizer.com
The ATP-binding cassette transporter A1 (ABCA1) encodes a membrane protein that promotes cholesterol and phospholipid efflux from cells. Mutations in ABCA1 lead to HDL deficiency and tissue accumulation of macrophages in patients with homozygous Tangier disease. In this study, we examined whether the complete absence of ABCA1 or selected inactivation in macrophages is accompanied by an increase in atherosclerotic lesion progression in hypercholesterolemic apolipoprotein E–deficient (apoE-/-) mice and LDLR receptor–deficient (LDLr-/-) mice. The absence of ABCA1 led to reduced plasma cholesterol levels in both the apoE-/- and LDLr-/- mice, along with severe skin xanthomatosis characterized by marked foamy macrophages and cholesterol ester accumulation. However, the complete absence of ABCA1 did not affect the development, progression, or composition of atherosclerotic lesions in either the LDLr-/- or the apoE-/- mice fed a chow or atherogenic diet. In contrast, bone marrow transplantation studies demonstrated that the selective inactivation of ABCA1 in macrophages markedly increased atherosclerosis and foam cell accumulation in apoE-/-. Taken together, these findings demonstrate that the complete absence of ABCA1 has a major impact on plasma lipoprotein homeostasis, and the proposed antiatherogenic effect resulting from ABCA1 deficiency is compensated by a less atherogenic profile. ABCA1 deficiency in macrophages, however, demonstrates the antiatherogenic properties of ABCA1 independent of plasma lipids and HDL levels.
Key Words: ABCA1 • atherosclerosis • xanthomatosis • HDL
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J. D. Mulligan, M. T. Flowers, A. Tebon, J. J. Bitgood, C. Wellington, M. R. Hayden, and A. D. Attie ABCA1 Is Essential for Efficient Basolateral Cholesterol Efflux during the Absorption of Dietary Cholesterol in Chickens J. Biol. Chem., April 4, 2003; 278(15): 13356 - 13366. [Abstract] [Full Text] [PDF]
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Y. Sun, M. Hao, Y. Luo, C.-p. Liang, D. L. Silver, C. Cheng, F. R. Maxfield, and A. R. Tall Stearoyl-CoA Desaturase Inhibits ATP-binding Cassette Transporter A1-mediated Cholesterol Efflux and Modulates Membrane Domain Structure J. Biol. Chem., February 14, 2003; 278(8): 5813 - 5820. [Abstract] [Full Text] [PDF]
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B. Feng and I. Tabas ABCA1-mediated Cholesterol Efflux Is Defective in Free Cholesterol-loaded Macrophages. MECHANISM INVOLVES ENHANCED ABCA1 DEGRADATION IN A PROCESS REQUIRING FULL NPC1 ACTIVITY J. Biol. Chem., November 1, 2002; 277(45): 43271 - 43280. [Abstract] [Full Text] [PDF]
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S. T. Reddy, S. Hama, C. Ng, V. Grijalva, M. Navab, and A. M. Fogelman ATP-Binding Cassette Transporter 1 Participates in LDL Oxidation by Artery Wall Cells Arterioscler Thromb Vasc Biol, November 1, 2002; 22(11): 1877 - 1883. [Abstract] [Full Text] [PDF]
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 R. K. Tangirala, E. D. Bischoff, S. B. Joseph, B. L. Wagner, R. Walczak, B. A. Laffitte, C. L. Daige, D. Thomas, R. A. Heyman, D. J. Mangelsdorf, et al. Identification of macrophage liver X receptors as inhibitors of atherosclerosis PNAS, September 3, 2002; 99(18): 11896 - 11901. [Abstract] [Full Text] [PDF]
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