This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tall, A. R. Articles by Lalanne, F. Search for Related Content PubMed PubMed Citation Articles by Tall, A. R. Articles by Lalanne, F.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1484.)
© 2003 American Heart Association, Inc.

Editorial

Phospholipid Transfer Protein and Atherosclerosis

Alan R. Tall; Florent Lalanne

From the Division of Molecular Medicine, Department of Medicine, Columbia University, New York.

Correspondence to Dr Alan Tall, Columbia University, Division of Molecular Medecine, Department of Medecine, P&S 8–401, 630 W 168th St, New York, NY 10032. E-mail art1@columbia.edu

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

Genetic studies in humans and mice show that two related plasma lipid transfer proteins (cholesteryl ester transfer protein [CETP] and phospholipid transfer protein [PLTP]) have distinct roles in lipoprotein metabolism, despite their homology.¹ In human homozygous CETP deficiency, HDL levels are massively elevated, and LDL levels are moderately decreased.² While a human PLTP deficiency state has not been described, PLTP-/- mice have 50% reductions in HDL levels, indicating the essential role of PLTP in transferring phospholipids from triglyceride-carrying lipoproteins into HDL.³ When crossed with apoE-/- mice, or apoB transgenic mice, PLTP deficiency results in reductions in apoB lipoproteins, revealing a role of intracellular PLTP in the hepatic secretion of apoB lipoproteins.⁴

See page 1601

Crosses of PLTP deficient mice into apoB transgenic, apoE-/-, or LDL R-/- backgrounds resulted in diminished atherosclerosis in all three of these standard mouse atherosclerosis models.⁴ In part this was related to the reduction of levels of apoB containing lipoproteins seen in apoB transgenic and apoE-/- mice. However, an anti-atherogenic effect of PLTP deficiency was also seen in LDL R-/- mice, despite a lack of reduction in apoB lipoprotein levels. A possible clue to understanding this unexpected observation was the finding that PLTP could facilitate the in vitro transfer of vitamin E from triglyceride rich lipoproteins (TRL) into HDL.⁵ An analysis of vitamin E revealed a build-up of levels in VLDL and LDL of PLTP deficient mice, associated with a reduction in susceptibility of apoB lipoproteins to Cu-mediated oxidation in vitro. Moreover, there was a reduction . . . [Full Text of this Article]

This article has been cited by other articles:

				L. Shelly, L. Royer, T. Sand, H. Jensen, and Y. Luo Phospholipid transfer protein deficiency ameliorates diet-induced hypercholesterolemia and inflammation in mice J. Lipid Res., April 1, 2008; 49(4): 773 - 781. [Abstract] [Full Text] [PDF]