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A more recent version of this article appeared on March 1, 2006

Papers In Press, published online ahead of print December 7, 2005
J. Lipid Res., doi:10.1194/jlr.M500444-JLR200
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Submitted on October 7, 2005
Revised on November 11, 2005
Accepted on December 7, 2005

Hepatic scavenger receptor BI-mediated cholesteryl ester selective uptake occurs with unaltered efficiency in the absence of cellular energy

Chris J. Harder, Gerard Vassiliou, Heidi M. McBride, and Ruth McPherson

Lipoprotein and Atherosclerosis Group, University of Ottawa Heart Institute, Ottawa, Ontario K1Y 4W7

Corresponding Author: rmcpherson{at}ottawaheart.ca

Scavenger receptor BI (SR-BI) plays a critical role in the delivery of high-density lipoprotein (HDL) cholesterol and cholesteryl esters (CE) to liver and steroidogenic tissues by a selective process that does not result in significant degradation of HDL protein. Recently, SR-BI- mediated endocytosis and recycling of HDL have been demonstrated. However, it remains unclear whether efficient SR-BI-mediated selective uptake occurs strictly at the plasma membrane or at additional sites along its endocytic itinerary. To examine the requirement for SR-BI endocytosis in HDL selective uptake, we determined the effects of energy depletion on the levels of cell-associated HDL protein and CE in primary mouse hepatocytes. Compared to CHO cells, we observed a much larger energy-dependent effect on CE uptake in primary mouse hepatocytes. Although varying the levels of caveolin-1 and carboxyl ester lipase altered the efficiency of selective uptake, neither was able to account for the energy dependent component of HDL-CE uptake. Finally, we demonstrate that the hepatocyte-specific, energy-dependent effect on HDL-apoAI and -CE uptake are independent of SR-BI and are not required to achieve efficient SR-BI mediated selective uptake of CE. Taken together, these data support the conclusion that neither the intracellular trafficking of HDL nor any energy-dependent cellular process affect the ability of the cell to maximally acquire CE through SR-BI-mediated selective uptake from HDL.


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