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Human Molecular Genetics Advance Access published online on April 28, 2004
Human Molecular Genetics, doi:10.1093/hmg/ddh145
© 2004 by Oxford University Press
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Article

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

Ewa Ninio 1*, David Tregouet 2, Jean-Luc Carrier 2, Dominique Stengel 2, Christoph Bickel 3, Caire Perret 2, Hans J. Rupprecht 3, François Cambien 2, Stefan Blankenberg 4, Laurence Tiret 2, AtheroGene Investigators

1 INSERM U525/IFR14 Coeur Muscle Vaisseaux and Université P.M. Curie/Faculté de Médecine Pitié-Salpêtrière, 91 bd de l'Hôpital 75634 Paris cedex 13 - France
2 INSERM U525/IFR14 Coeur Muscle Vaisseaux and Université P.M. Curie/Faculté de Médecine, Paris, France
3 Department of Medicine II, Johannes Gutenberg-University Mainz, Mainz, Germany
4 INSERM U525/IFR14 Coeur Muscle Vaisseaux and Université P.M. Curie/Faculté de Médecine, Paris, France; Department of Medicine II, Johannes Gutenberg-University Mainz, Mainz, Germany

* To whom correspondence should be addressed. E-mail: ninio{at}chups.jussieu.fr.


  Abstract

Oxidation of low density lipoproteins is an initial step of atherogenesis which generates proinflammatory 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 event, 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 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.


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