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Published Online
on August 23, 2007

Arteriosclerosis, Thrombosis, and Vascular Biology. 2007
Published online before print August 23, 2007, doi: 10.1161/ATVBAHA.107.151753
A more recent version of this article appeared on November 1, 2007
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Submitted on April 20, 2007
Accepted on August 1, 2007

Cholesterol Accumulation Is Increased in Macrophages of Phospholipid Transfer Protein-Deficient Mice. Normalization by Dietary Alpha-Tocopherol Supplementation

Nicolas Ogier ; Alexis Klein ; Valérie Deckert ; Anne Athias ; Ginette Bessède ; Naig Le Guern ; Laurent Lagrost ; and Catherine Desrumaux *

From INSERM U866, Centre de Recherche INSERM, IFR Santé-STIC, Faculté de Médecine, Université de Bourgogne, Dijon, France.

* To whom correspondence should be addressed. E-mail: Catherine.Desrumaux{at}u-bourgogne.fr.

Objective—Phospholipid transfer protein (PLTP) is a multifunctional, extracellular lipid transport protein that plays a major role in lipoprotein metabolism and atherosclerosis. Recent in vivo studies suggested that unlike systemic PLTP, macrophage-derived PLTP would be antiatherogenic. The present study aimed at characterizing the atheroprotective properties of macrophage-derived PLTP.

Methods and Results—Peritoneal macrophages were isolated from PLTP-deficient and wild-type mice and their biochemical characteristics were compared. It is shown that macrophages isolated from PLTP-deficient mice have increased basal cholesterol content and accumulate more cholesterol in the presence of LDL compared with wild-type cells. Cholesterol parameters in macrophages of PLTP-deficient mice were normalized by dietary {alpha}-tocopherol supplementation.

Conclusions—The antiatherogenic properties of macrophage-derived PLTP are related at least in part to its ability to reduce cholesterol accumulation in macrophages through changes in the {alpha}-tocopherol content and oxidative status of the cells.


Key words: phospholipid transfer protein • vitamin E • tocopherol • macrophage




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J. F. Oram, G. Wolfbauer, C. Tang, W. S. Davidson, and J. J. Albers
An Amphipathic Helical Region of the N-terminal Barrel of Phospholipid Transfer Protein Is Critical for ABCA1-dependent Cholesterol Efflux
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