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

• Main Authors: Veneracion G. Cabana, Ning Feng, Catherine A. Reardon, John Lukens, Nancy R. Webb, Frederick C. de Beer, Godfrey S. Getz
• Format: Article
• Language: English
• Published: Elsevier 2004-02-01
• Series: Journal of Lipid Research
• Subjects: apolipoprotein A-I; high density lipoprotein; acute-phase response
• Online Access: http://www.sciencedirect.com/science/article/pii/S0022227520319040

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.