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on October 30, 2003

Arteriosclerosis, Thrombosis, and Vascular Biology. 2003
Published online before print October 30, 2003, doi: 10.1161/01.ATV.0000104029.74961.f5
A more recent version of this article appeared on March 1, 2004
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Right arrow Lipid and lipoprotein metabolism

Submitted on September 21, 2003
Accepted on October 16, 2003

Formation and Metabolism of Prebeta-Migrating, Lipid-Poor Apolipoprotein A-I

Kerry-Anne Rye and Philip J. Barter *

From the The Heart Research Institute, Sydney, Australia.

* To whom correspondence should be addressed. E-mail: p.barter{at}hri.org.au.

Objective--The preferred extracellular acceptor of cell phospholipids and unesterified cholesterol in the process mediated by the ATP-binding cassette A1 (ABCA1) transporter is a monomolecular, prebeta-migrating, lipid-poor or lipid-free form of apolipoprotein (apo) A-I. This monomolecular form of apoA-I is quite distinct from the prebeta-migrating, discoidal high-density lipoprotein (HDL) that contains two or three molecules of apoA-I per particle and which are present as minor components of the HDL fraction in human plasma. The mechanism of the ABCA1-mediated efflux of phospholipid and cholesterol from cells has been studied extensively. In contrast, much less attention has been given to the origin and subsequent metabolism of the acceptor lipid-free/lipid-poor apoA-I. There is a substantial body of evidence from studies conducted in vitro that a monomolecular, lipid-free/lipid-poor form of apoA-I dissociates from HDL during the remodelling of high-density lipoproteins by plasma factors such as cholesteryl ester transfer protein, hepatic lipase, and phospholipid transfer protein. The rate at which apoA-I dissociates from HDL is influenced by the phospholipid composition of the particles and by the presence of apoA-II. This review describes current knowledge regarding the formation, metabolism, and regulation of monomolecular, lipid-free/lipid-poor apoA-I in plasma.




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