J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on December 1, 2007

Papers In Press, published online ahead of print August 29, 2007
J. Lipid Res., doi:10.1194/jlr.M700020-JLR200
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Submitted on January 16, 2007
Revised on August 28, 2007
Accepted on August 28, 2007

Atherogenic, enlarged and dysfunctional HDL in human PLTP/ApoAI double transgenic mice

Matthijs Moerland, Hannelore Samyn, Teus van Gent, Matti Jauhiainen, Jari Metso, Rien van Haperen, Frank Grosveld, Arie van Tol, and Rini de Crom

Cell Biology & Genetics, Erasmus University Medical Center, Rotterdam 3015 GD

Corresponding Author: m.decrom{at}erasmusmc.nl

In low-density lipoprotein receptor (LDLR) deficient mice, overexpression of human plasma phospholipid transfer protein (hPLTP) results in increased atherosclerosis. PLTP strongly decreases high-density lipoprotein (HDL) levels, and might alter the anti-atherogenic properties of HDL particles. To study the potential interaction between human PLTP and apolipoprotein AI, double transgenic animals (hPLTPtg/hApoAItg) were compared with hApoAItg mice. PLTP activity was 4.5-fold increased. Total plasma TC and PL were decreased. Average HDL size (analyzed by gel filtration) increased strongly, hPLTPtg/hApoAItg mice having very large, LDL-sized, HDL particles. Also after density gradient ultracentrifugation, a substantial part of the ApoAI containing lipoproteins in hPLTPtg/hApoAItg mice was found in the LDL density range. In cholesterol efflux studies from macrophages, HDL isolated from hPLTPtg/hApoAItg mice was less efficient than HDL isolated from hApoAItg mice. Furthermore, it was found that the largest subfraction of the HDL particles present in hPLTPtg/hApoAItg mice was markedly inferior as cholesterol acceptor, as no labeled cholesterol was transferred to this fraction. In an LDLR deficient background, the hPLTP expressing mouse line showed a 2.2-fold increased atherosclerotic lesion area. These data demonstrate that the action of hPLTP in presence of hApoAI results in the formation of a dysfunctional HDL subfraction, which is less efficient in the uptake of cholesterol from cholesterol-laden macrophages.


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