
Association of the −92C/G and 807C/T Polymorphisms of the α 2 Subunit Gene With Human Platelets α 2 β 1 Receptor Density
Author(s) -
Nadine Ajzenberg,
Clarisse Berroëta,
Ivan Philip,
Bernard Grandchamp,
Pierre Ducellier,
Virginie Huart,
Patrice Verpillat,
MarieClaude Guillin,
Joëlle Bénessiano
Publication year - 2005
Publication title -
arteriosclerosis, thrombosis, and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/01.atv.0000173308.13054.4f
Subject(s) - gene , protein subunit , genetics , platelet , association (psychology) , biology , microbiology and biotechnology , psychology , immunology , psychotherapist
Objective— Platelet adhesion to the subendothelial tissue via the collagen receptor α2 β1 is a crucial event in vascular biology. Although evidence has been provided that the number of platelets α2 β1 copies is genetically determined, the molecular change primary responsible has not been yet elucidated. The aim of our present study was to investigate the effect of combined polymorphisms within both regulatory (−52C/T and −92C/G) and coding regions (807C/T and 1648A/G) of the α2 subunit gene on human platelets α2 β1 receptor density and/or susceptibility to coronary artery disease (CAD).Methods and Results— Among 254 cardiac surgery patients, no evidence was found for an association between the α2 subunit gene polymorphisms and CAD. In contrast, in a subgroup of 113 patients, we observed a significant association between all polymorphisms except −52C/T and α2 β1 receptor level. Furthermore, when 3 groups of patients were defined according to the tertiles of platelets α2 β1 copies, the −92C/807T haplotype was more frequent in the group of patients with high α2 β1 receptor level.Conclusion— These results suggest that an individual effect of each polymorphism located either in the coding or promoter sequence of the α2 gene may act in combination to modulate variations in platelets α2 β1 receptor density.