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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:2175.)
© 2006 American Heart Association, Inc.

Editorials

Is Two out of Three Enough for ABCG1?

Linda K. Curtiss

From The Scripps Research Institute, Department of Immunology, La Jolla, Calif.

Correspondence to Linda K. Curtiss, PhD, The Scripps Research Institute, Department of Immunology, IMm-17, 10550 North Torrey Pines Rd, La Jolla, CA 92037. E-mail lcurtiss@scripps.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Macrophages have the right tools to synthesize all the free cholesterol they need. If macrophages also could degrade cholesterol when they have too much, the concept of in vivo reverse cholesterol transport (RCT) would be irrelevant. Fortunately for those of us who do research in this area, the ability of macrophages to closely regulate their cellular cholesterol levels is accomplished not by cellular degradation, but by multiple complex cholesterol sensing regulatory pathways including enzyme systems for synthesizing it, esterifying it, and actively transporting it out of the cell. RTC can be defined as the transport of cholesterol from peripheral cells such as macrophages to circulating plasma lipoproteins that subsequently deliver the cholesterol to the liver for biliary excretion.¹ Active transport of cholesterol out of cells to lipid-poor or lipid-free apolipoprotein AI (apoAI) is accomplished by the LXR-inducible ATP binding cassette transporter, ABCA1.² This transporter exports both cellular cholesterol and phospholipid. Whereas ABCA1 exports cholesterol and phospholipid to lipid-free apolipoproteins, another more recently described LXR-inducible transporter, ABCG1 actively exports cellular cholesterol to high density lipoproteins (HDL) and other extracellular phospholipid-containing acceptors.³ Recently, it has been suggested that ABCA1 and ABCG1 work in concert to export cellular phospholipid and cholesterol. ABCA1 generates extracellular nascent or discoidal HDL, which then becomes an acceptor for ABCG1-mediated additional cholesterol efflux.⁴ Although this idea is logically sound, the relevant contributions of ABCA1 and ABCG1 to macrophage cholesterol export are still not completely understood.

See pages 2295, 2301, 2308

Because ABCG1 is a key regulator of . . . [Full Text of this Article]

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