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Journal of Lipid Research, Vol. 45, 317-325, February 2004
Copyright © 2004 by American Society for Biochemistry and Molecular Biology

Influence of apoA-I and apoE on the formation of serum amyloid A-containing lipoproteins in vivo and in vitro

Veneracion G. Cabana^*, Ning Feng^*, Catherine A. Reardon^*, John Lukens^*, Nancy R. Webb, Frederick C. de Beer and Godfrey S. Getz^1,*

^* Department of Pathology, University of Chicago, Chicago, IL 60637
Department of Internal Medicine, University of Kentucky Medical Center, Lexington, KY 40536

¹ To whom correspondence should be addressed. e-mail: g-getz{at}uchicago.edu

Serum amyloid A (SAA) circulates bound to HDL₃ during the acute-phase response (APR), and recent evidence suggests that elevated levels of SAA may be a risk factor for cardiovascular disease. In this study, SAA-HDL was produced in vivo during the APR and without the APR by injection of an adenoviral vector expressing human SAA-1. SAA-HDL was also produced in vitro by incubating mouse HDL with recombinant mouse SAA and by SAA-expressing cultured hepatoma cells. Whether produced in vivo or in vitro, SAA-HDL floated at a density corresponding to that of human HDL₃ (d 1.12 g/ml) separate from other apolipoproteins, including apolipoprotein A-I (apoA-I; d 1.10 g/ml) when either apoA-I or apolipoprotein E (apoE) was present. In the absence of both apoA-I and apoE, SAA was found in VLDL and LDL, with low levels in the HDL and the lipid-poor fractions suggesting that other HDL apolipoproteins are incapable of facilitating the formation of SAA-HDL.

We conclude that SAA does not exist in plasma as a lipid-free protein. In the presence of HDL-associated apoA-I or apoE, SAA circulates as SAA-HDL with a density corresponding to that of human HDL₃. In the absence of both apoA-I and apoE, SAA-HDL is not formed and SAA associates with any available lipoprotein.

Abbreviations: adv-huSAA1, recombinant adenovirus expressing human SAA1; APR, acute-phase response; EA^-/-, mice deficient in both the apoA-I and apoE genes; LPS, lipopolysaccharide; RE^-/-, mice deficient in both the apoE gene and the recombination activation gene 2; r-moSAA, recombinant mouse SAA; SAA, serum amyloid A

Supplementary key words apolipoprotein A-I • high density lipoprotein • acute-phase response

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