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Papers In Press, published online ahead of print November 1, 2003
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Department of Pathology, University of Chicago, Chicago, IL 60637-1470
Corresponding Author: getz{at}delphi.bsd.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 the density corresponding to human HDL3 (d1.12 g/ml) separate from other apoproteins including apoA-I (d1.10 g/ml) when either apoA-I or 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 apoproteins 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 human HDL3. In the absence of both apoA-I and apoE, SAA-HDL is not formed and SAA associates with any available lipoprotein.
Revised on October 17, 2003
Accepted on October 21, 2003
Influence of apoA-I and apoE on the formation of SAA-containing lipoproteins in vivo and in vitro
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