on November 3, 2005
Published online before print November 3, 2005, doi: 10.1161/01.ATV.0000194291.94269.5a
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Submitted on August 25, 2005
Accepted on October 19, 2005
What Is So Special About Apolipoprotein AI in Reverse Cholesterol Transport?
Linda K. Curtiss *;
From the Department of Immunology (L.K.C., D.T.V., N.J.H.), The Scripps Research Institute, La Jolla, Calif; The Heart Research Institute, Ltd (K-A.R.), Camperdown, Sydney, New South Wales, Australia; the Department of Medicine (K-A.R.), University of Sydney, New South Wales, Australia; and the Department of Medicine (K-A.R.), University of Melbourne, Victoria, Australia.
* To whom correspondence should be addressed. E-mail: lcurtiss{at}scripps.edu.
Abstract--An initial step in reverse cholesterol transport is the movement of unesterified cholesterol from peripheral cells to high-density lipoproteins (HDLs). This transfer usually occurs in extracellular spaces, such as the subendothelial space of a vessel wall, and is promoted by the interaction of lipid-free or lipid-poor apolipoprotein (apo)AI with ATP binding cassette A1 cellular transporters on macrophages (M
). Because HDL does not interact with M ATP binding cassette A1 and apoAI is not synthesized by macrophages, this apoAI must be generated from spherical HDL. In this brief review, we propose that spherical apoAI is derived from HDL by remodeling events that are accomplished by proteins secreted by cholesteryl ester-loaded foam cells, including the lipid transfer proteins, phospholipid transfer protein, and cholesteryl ester transfer protein, and the triglyceride hydrolases hepatic lipase and lipoprotein lipase.
Key words: apoprotein AI • PLTP • CETP • HL • macrophage
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