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J. Lipid Res.
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A more recent version of this article appeared on July 1, 2005

Papers In Press, published online ahead of print April 16, 2005
J. Lipid Res., doi:10.1194/jlr.M500085-JLR200
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Submitted on March 1, 2005
Revised on March 28, 2005
Accepted on April 12, 2005

Loss of G2A promotes macrophage accumulation in atherosclerotic lesions of low-density lipoprotein receptor-deficient mice

Brian W. Parks, Ginger P. Gambill, Aldons J. Lusis, and Janusz H. S. Kabarowski

Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294-2170

Corresponding Author: janusz{at}uab.edu

Lysophosphatidylcholine is considered a major pro-atherogenic component of oxidized low-density lipoprotein based on its pro-inflammatory actions in vitro. Lysophosphatidylcholine stimulates macrophage and T cell chemotaxis via the G protein-coupled receptor G2A and may thus promote inflammatory cell infiltration during atherosclerotic lesion development. However, G2A also mediates pro-apoptotic effects of lysophosphatidylcholine and may therefore promote death of inflammatory cells within developing lesions. To determine how these effects of lysophosphatidylcholine modify atherogenesis, we examined atherosclerotic lesion development in G2A-sufficient and G2A-deficient low-density lipoprotein receptor knockout mice. Although lysophosphatidylcholine species capable of activating G2A-dependent responses were increased during lesion development, G2A-deficient mice developed lesions similar in size to those in their G2A-sufficient counterparts. Loss of G2A during atherosclerotic lesion development did not reduce macrophage and T cell infiltration but instead resulted in increased lesional macrophage content associated with reduced numbers of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeled cells and decreased collagen deposition. These data indicate that the ability of lysophosphatidylcholine to stimulate macrophage and T cell chemotaxis via G2A is not manifested in vivo and G2A-mediated pro-apoptotic rather than chemotactic action is most penetrant during atherogenesis and may modify the stability of atherosclerotic lesions by promoting macrophage death.


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