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J. Biol. Chem., Vol. 278, Issue 25, 22530-22536, June 20, 2003

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Apolipoprotein A-II Inhibits High Density Lipoprotein Remodeling and Lipid-poor Apolipoprotein A-I Formation^*

Kerry-Anne Rye   ¶, Kevin Wee  , Linda K. Curtiss || **, David J. Bonnet || and Philip J. Barter   

From the Lipid Research Laboratory, Hanson Institute, Adelaide, South Australia 5000, Australia, ^||Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, and Department of Medicine, University of Adelaide, Royal Adelaide Hospital, South Australia 5000, Australia

The high density lipoproteins (HDL) in human plasma are classified on the basis of apolipoprotein composition into those containing apolipoprotein (apo) A-I but not apoA-II, (A-I)HDL, and those containing both apoA-I and apoA-II, (A-I/A-II)HDL. Cholesteryl ester transfer protein (CETP) transfers core lipids between HDL and other lipoproteins. It also remodels (A-I)HDL into large and small particles in a process that generates lipid-poor, pre--migrating apoA-I. Lipid-poor apoA-I is the initial acceptor of cellular cholesterol and phospholipids in reverse cholesterol transport. The aim of this study is to determine whether lipid-poor apoA-I is also formed when (A-I/A-II)rHDL are remodeled by CETP. Spherical reconstituted HDL that were identical in size had comparable lipid/apolipoprotein ratios and either contained apoA-I only, (A-I)rHDL, or (A-I/A-II)rHDL were incubated for 0–24 h with CETP and Intralipid^®. At 6 h, the apoA-I content of the (A-I)rHDL had decreased by 25% and there was a concomitant formation of lipid-poor apoA-I. By 24 h, all of the (A-I)rHDL were remodeled into large and small particles. CETP remodeled 32% (A-I/A-II)rHDL into small but not large particles. Lipid-poor apoA-I did not dissociate from the (A-I/A-II)rHDL. The reasons for these differences were investigated. The binding of monoclonal antibodies to three epitopes in the C-terminal domain of apoA-I was decreased in (A-I/A-II)rHDL compared with (A-I)rHDL. When the (A-I/A-II)rHDL were incubated with Gdn-HCl at pH 8.0, the apoA-I unfolded by 15% compared with 100% for the apoA-I in (A-I)rHDL. When these incubations were repeated at pH 4.0 and 2.0, the apoA-I in the (A-I)rHDL and the (A-I/A-II)rHDL unfolded completely. These results are consistent with salt bridges between apoA-II and the C-terminal domain of apoA-I, enhancing the stability of apoA-I in (A-I/A-II)rHDL and possibly contributing to the reduced remodeling and absence of lipid poor apoA-I in the (A-I/A-II)rHDL incubations.

Received for publication, December 30, 2002 , and in revised form, March 31, 2003.

^* This work was supported by the National Health and Medical Research Council of Australia. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Present address: The Heart Research Institute, 145 Missenden Rd., Camperdown, New South Wales 2050, Australia.

^** Supported by National Institutes of Health Grant HL43815.

^¶ Principal Career Research Fellow of the National Heart Foundation of Australia. To whom correspondence should be addressed. Tel.: 61-2-9550-3560; Fax: 61-2-9550-3302; E-mail: karye{at}ozemail.com.au.

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