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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2016-2017
doi: 10.1161/01.ATV.0000186042.94668.2b
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2016.)
© 2005 American Heart Association, Inc.


Editorials

A Role for the Pregnane X Receptor in High-Density Lipoprotein Metabolism

Gregory S. Shelness; Lawrence L. Rudel

From the Lipid Sciences Research Program, Department of Pathology, Wake Forest University School of Medicine, Winston-Salem, NC.

Correspondence to Lawrence L. Rudel, Lipid Sciences Research Program, Department of Pathology, Wake Forest University School of Medicine, Winston-Salem, NC 27157. E-mail lrudel@wfubmc.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

High-density lipoprotein (HDL) cholesterol is widely recognized as the good plasma cholesterol for coronary heart disease and is believed to be responsible for cholesterol transport from peripheral tissues back to the liver, the central clearing house for cholesterol in the body. Interestingly, the liver is also a major site for HDL production, although the process of particle assembly is believed to occur intravascularly.1–4 ApoA-I is secreted by the liver in lipid-poor form and then interacts with ATP-binding cassette protein A1 (ABCA1) in liver and peripheral tissues to acquire phospholipids and cholesterol, forming a discoidal HDL intermediate sometimes referred to as pre–ß-HDL. These particles are excellent substrates for the liver-derived plasma enzyme lecithin:cholesterol acyltransferase. Using the sn-2 fatty acids of the particle-associated phosphatidylcholine, lecithin:cholesterol acyltransferase catalyzes the esterification of cholesterol, which is partially derived from peripheral tissues. This reaction produces the cholesteryl esters (CE) that form the neutral lipid core of the mature spherical HDL particles. In addition to whole HDL particle uptake by the liver, the CE of mature HDL can also be removed by the liver through a process of selective CE uptake via scavenger receptor-class B type I (SR-BI). Both uptake mechanisms result in a directional flux of cholesterol from the plasma compartment to the liver. Some of the HDL-derived cholesterol becomes part of the hepatic pool that is used for bile acid formation (with subsequent secretion together with cholesterol into bile). Bile acid synthesis represents the primary pathway of cholesterol catabolism in the body. In addition, a . . . [Full Text of this Article]


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Expression of the Pregnane X Receptor in Mice Antagonizes the Cholic Acid–Mediated Changes in Plasma Lipoprotein Profile
David Masson, Laurent Lagrost, Anne Athias, Philippe Gambert, Cynthia Brimer-Cline, Lubin Lan, John D. Schuetz, Erin G. Schuetz, and Mahfoud Assem
Arterioscler Thromb Vasc Biol 2005 25: 2164-2169. [Abstract] [Full Text] [PDF]



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