Abstract
SAA, HDL biogenesis, and inflammation
Highlights
The understanding of Tangier disease has, over the last decade, focused attention on the role of the ABC transporter ABCA1 in the biogenesis of HDL [1]
They studied ABCA1 knockout animals and the cells derived from them for further cell-based studies. These experiments furnish valuable new information about the complex relationship between serum amyloid A (SAA), ABCA1, HDL, and the properties of SAA, they raise new questions that would be appropriate for further study. They demonstrate that, unlike the situation in normal mice, in which SAA is largely associated with HDL after the induction of SAA expression by injection of lipopolysaccharide (LPS), in the absence of ABCA1 there is little or no HDL and the small amount of SAA present in plasma is mostly found in the VLDL/LDL fraction
The amount of SAA secreted from primary hepatocytes derived from LPS-treated knockout animals is significantly lower than that secreted from wildtype mice, and all of the SAA secreted from the knockout hepatocytes was recovered as lipid-free protein
Summary
The understanding of Tangier disease has, over the last decade, focused attention on the role of the ABC transporter ABCA1 in the biogenesis of HDL [1]. In this issue of the Journal of Lipid Research, Hu and colleagues [7] examine, in a series of elegant experiments, the interaction between SAA, HDL biogenesis, and the dependence of the formation of SAA-HDL on ABCA1. Because hepatocytes from wild-type mice are able to secrete SAA in association with HDL-like particles, and comparable levels of apoA-I were secreted from the wild-type and knockout hepatocytes.
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