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Papers In Press, published online ahead of print November 4, 2002
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Submitted on October 18, 2002
Molecular Disease Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892
Corresponding Author: silvia{at}mdb.nhlbi.nih.gov
The current model for reverse cholesterol transport (RCT) proposes that HDL transports excess cholesterol derived primarily from peripheral cells to the liver for removal. However, recent studies in ABCA1 transgenic mice suggest that the liver itself may be a major source of HDL-C. To directly investigate the hepatic contribution to plasma HDL-C levels we generated an adenovirus (rABCA1-GFP-AdV) that targets expression of mouse ABCA1-GFP in vivo to the liver. Compared to mice injected with control AdV, infusion of rABCA1-GFP-AdV into C57Bl/6 mice resulted in increased expression of mouse ABCA1 mRNA and protein in the liver. ApoA-I dependent cholesterol efflux was increased 2.6-fold in primary hepatocytes isolated one day after rABCA1-GFP-AdV infusion. Hepatic ABCA1 expression in C57Bl/6 mice (n=15) mice raised baseline levels of TC, PL, FC, HDL-C, apoE and apoA-I by 150-300% (p<0.05 all). ABCA1 expression led to significant compensatory changes in expression of genes that increase hepatic cholesterol, including HMGCoA reductase (3.5-fold), LDLr (2.1-fold) and LRP (5-fold) in the liver. These combined results demonstrate that ABCA1 plays a key role in hepatic cholesterol efflux, inducing pathways that modulate cholesterol homeostasis in the liver, and establish the liver as a major source of plasma HDL-C.
Revised on November 4, 2002
Accepted on October 30, 2002
Role of the hepatic ABCA1 transporter in modulating intrahepatic cholesterol and plasma HDL-cholesterol concentrations
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