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Human Molecular Genetics Advance Access originally published online on April 28, 2004
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Human Molecular Genetics, 2004, Vol. 13, No. 13 1341-1351
DOI: 10.1093/hmg/ddh145
Human Molecular Genetics, Vol. 13, No. 13 © Oxford University Press 2004; all rights reserved

Platelet-activating factor-acetylhydrolase and PAF-receptor gene haplotypes in relation to future cardiovascular event in patients with coronary artery disease

Ewa Ninio1,*, David Tregouet1, Jean-Luc Carrier1, Dominique Stengel1, Christoph Bickel2, Claire Perret1, Hans J. Rupprecht2, François Cambien1, Stefan Blankenberg1,2 and Laurence Tiret1 for the AtheroGene Investigators

1INSERM U525/IFR14 Coeur Muscle Vaisseaux and Université PM Curie/Faculté de Médecine Pitié-Salpêtrière, Paris, France and 2Department of Medicine II, Johannes Gutenberg-University Mainz, Mainz, Germany

Received February 26, 2004; Revised April 14, 2004; Accepted April 21, 2004

Oxidation of low density lipoproteins is an initial step of atherogenesis that generates pro-inflammatory phospholipids, including platelet-activating factor (PAF) and its analogs. PAF is degraded by PAF-acetylhydrolase (PAF-AH), a circulating enzyme having both pro- and anti-inflammatory activities. PAF-AH activity has been postulated to be a risk factor for coronary artery disease (CAD); however, whether PAF-AH has a causal role or is simply a marker of risk is unclear. The aim of this study was to relate the variability of the genes encoding PAF-AH (PLA2G7) and the PAF-receptor (PTAFR) to the risk of CAD and its complications. All polymorphisms located in putatively functional regions were investigated in a prospective cohort of CAD patients (n=1314) and a group of healthy controls (n=485). The whole gene variability was investigated in relation to case–control status, prospective cardiovascular outcome and plasma PAF-AH levels by means of haplotype analyses. All analyses indicated an effect of the PLA2G7/A379V polymorphism independent of the other polymorphisms. The V379 allele was less frequent in CAD patients than in controls and was associated with a lower risk of future cardiovascular events, suggesting that this allele might be protective against the development of CAD. The V379 allele was also associated with a weak increase of plasma PAF-AH activity that was unlikely to explain the protective effect of the allele on risk. A more likely interpretation is that the A379V polymorphism might modify the enzyme function towards a more anti-atherogenic form. Polymorphisms of the PTAFR gene were not related to any phenotype.

* To whom correspondence should be addressed at: INSERM U525, Faculté de Médecine Pitié-Salpêtrière, 91 bd de l'Hôpital, 75634 Paris cedex 13, France. Tel: +33 140779725; Fax: +33 140779768; Email: ninio{at}chups.jussieu.fr


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