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Papers In Press, published online ahead of print March 1, 2004
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Medicine and Biochemistry, University of Alberta, Edmonton, Alberta T6G 2S2
Corresponding Author: gordon.francis{at}ualberta.ca
High levels of expression of the ATP-binding cassette transporter A1 (ABCA1) in the liver, and the need to over- or under-express hepatic ABCA1 to impact plasma HDL levels in mice, suggest a major role of the liver in HDL formation and in determining circulating HDL levels. Cultured McArdle RH7777 hepatoma cells and primary rat and mouse hepatocytes were used to examine the role of hepatic ABCA1 in mediating the lipidation of apolipoprotein A-I for HDL particle formation. Exogenous apoA-I stimulated cholesterol efflux to the medium from primary rat and mouse hepatocytes, but not from ABCA1-deficient hepatocytes. ApoA-I induced the formation of new HDL particles and enhanced the lipidation of endogenously secreted murine apoA-I in ABCA1-expressing but not ABCA1-deficient hepatocytes. ABCA1-dependent cholesterol mobilization to apoA-I increased new cholesterol synthesis by hepatocytes, indicating depletion of the regulatory pool of hepatocyte cholesterol during HDL formation. Secretion of triacylglycerol and apoB was decreased following apoA-I incubation with primary ABCA1-expressing but not ABCA1-deficient hepatocytes. These results support a major role for hepatocyte ABCA1 in generating a critical pool of HDL precursor particles that enhance further HDL generation and passive cholesterol mobilization in the periphery. The results also suggest that diversion of hepatocyte cholesterol into the “reverse” cholesterol transport pathway may diminish cholesterol availability for apoB-containing lipoprotein secretion by the liver.
Revised on February 13, 2004
Accepted on February 24, 2004
ABCA1-dependent lipid efflux to apolipoprotein A-I mediates HDL particle formation and decreases VLDL secretion from primary rat and mouse hepatocytes
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