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A more recent version of this article appeared on January 1, 2008

Papers In Press, published online ahead of print October 10, 2007
J. Lipid Res., doi:10.1194/jlr.M700228-JLR200
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Submitted on May 15, 2007
Revised on October 5, 2007
Accepted on October 9, 2007

Macrophage phospholipid transfer protein (PLTP) is atheroprotective in LDLr-/- mice with systemic PLTP deficiency

David T. Valenta, Joshua J. Bulgrien, David J. Bonnet, and Linda K. Curtiss

Immunology, The Scripps Research Institute, La Jolla, CA 82037

Corresponding Author: lcurtiss{at}scripps.edu

Systemic phospholipid transfer protein (PLTP) is a recognized risk factor for coronary heart disease. In apolipoprotein E-deficient mice systemic PLTP deficiency is atheroprotective, whereas PLTP overexpression is pro-atherogenic. As expected, we also observed significantly smaller lesions (P < 0.0001) in hypercholesterolemic double mutant LDLr-/-PLTP-/- mice compared to LDLr-/- mice expressing systemic PLTP. To assess the specific contribution of only macrophage-derived PLTP to atherosclerosis progression, bone-marrow transplantations were performed in LDLr-/- mice that also lacked systemic PLTP. Groups of double mutant PLTP-/-LDLr-/- mice were irradiated with 1000 rad and injected with bone marrow (BM) cells collected from either PLTP-/- or wild type (WT) mice. When fed a high fat diet, BM cell expression of PLTP lowered plasma cholesterol of PLTP-/-LDLr-/- mice from 878 ± 220 mg/dl to 617 ± 183 mg/dl, and raised the HDL cholesterol levels from 54 ± 11 mg/dl to 117 ± 19 mg/dl. This lowered total plasma cholesterol and raised HDL cholesterol contributed to the significantly smaller atherosclerotic lesions in both aortas and heart sinus valves observed in these mice. Thus, unlike total systemic PLTP, locally produced macrophage-derived PLTP beneficially alters lipoprotein metabolism and reduces lesion progression in hyperlipidemic mice.


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[Abstract] [Full Text] [PDF]


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