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A more recent version of this article appeared on February 1, 2008

Papers In Press, published online ahead of print November 21, 2007
J. Lipid Res., doi:10.1194/jlr.M700402-JLR200
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Submitted on September 6, 2007
Revised on November 21, 2007
Accepted on November 21, 2007

Biogenesis of high density lipoprotein by serum amyloid A is dependent on ATP-binding cassette transporter A1- in the liver in vivo

Wei Hu, Sumiko Abe-Dohmae, Maki Tsujita, Noriyuki Iwamoto, Osamu Ogikubo, Takanobu Otsuka, Yositaka Kumon, and Shinji Yokoyama

Biochemistry, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601

Corresponding Author: bc.abedo{at}med.nagoya-cu.ac.jp

Serum amyloid A (SAA) was markedly increased in the plasma and in the liver upon acute inflammation induced by intraperitoneal injection of lipopolysaccharide (LPS) in mice, and SAA in the plasma was exclusively associated with HDL. In contrast, no HDL was present in the plasma and only a small amount of SAA was found in VLDL/LDL fraction (d < 1.063 g/ml) after induction of the inflammation in ATP-binding cassette transporter (ABC) A1-knockout (KO) mice although SAA increased in the liver. Primary hepatocytes isolated from the LPS-treated wild-type (WT) and ABCA1-KO mice both secreted SAA into the medium. SAA secreted from the WT hepatocytes was associated with HDL while SAA from ABCA1-KO hepatocytes was recovered in the fraction heavier than 1.21 g/ml. Behavior of apoA-I was same as SAA in the HDL biogenesis by WT and ABCA1-KO mice hepatocytes. Lipid-free SAA and apoA-I both stabilized ABCA1 and caused cellular lipid release in WT mice-derived fibroblasts, but not in ABCA1-KO mice-derived fibroblasts in vitro, when exogenously added. We concluded that both SAA and apoA-I generate HDL largely in hepatocytes only in the presence of ABCA1, likely being secreted in a lipid-free form to interact with cellular ABCA1. In the absence of ABCA1, non-lipidated SAA is seemingly removed rapidly from the extracellular space.


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G. S. Getz and C. A. Reardon
SAA, HDL biogenesis, and inflammation
J. Lipid Res., February 1, 2008; 49(2): 269 - 270.
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