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Association between Platelet Glycoprotein Ib‐α and Myocardial Infarction
Author(s) -
CANDORE GIUSEPPINA,
PIAZZA GIUSEPPINA,
CRIVELLO ANTONINO,
GRIMALDI MARIA PAOLA,
ORLANDO VALENTINA,
CARUSO MARCO,
CAIMI GREGORIO,
HOFFMANN ENRICO,
INCALCATERRA EGLE,
LIO DOMENICO,
CARUSO CALOGERO
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1386.011
Subject(s) - von willebrand factor , platelet membrane glycoprotein , platelet , platelet glycoprotein gpib ix complex , medicine , glycoprotein ib , restriction fragment length polymorphism , myocardial infarction , thrombosis , endocrinology , immunology , biology , genotype , genetics , gene
Myocardial infarction (AMI) is a complex multifactorial disorder. Platelet adhesion and thrombosis are pivotal events in the development of atherosclerotic lesions. Occlusive thrombus is almost exclusively initiated by plaque rupture and adhesion of platelets to subendothelial von Willebrand factor (vWf) by its specific platelet receptor, the α‐chain of glycoprotein (GP) Ib‐IX‐V complex of the human platelet‐specific antigens (HPA). Two polymorphisms have been reported in the sequence of GPIb‐α. The first, a C/T transition at nucleotide 1018 results in an amino acid dimorphism (Thr/Met) at residue 145 of GPIb‐α, which is located within the vWF‐binding domain of the receptor. The second is a T/C polymorphism in the Kozak sequence at position −5 from the initiator ATG. This affects the receptor density on the platelet surface. We assessed 1018 C/T and −5 T/C Kozak polymorphisms to see whether they are associated with AMI in homogeneous populations of Sicilian patients with AMI. To this end, we have analyzed the distribution of 1018 C/T and −5 T/C Kozak polymorphisms in 105 young Sicilian patients (<46 years) and 110 healthy age‐related controls, by PCR–SSP and PCR–RFLP. Our results demonstrate no significant differences in the frequency of 1018 C/T and −5 T/C Kozak polymorphism between patients with AMI and controls. Stratifying by gender, there is no difference between male and female patients and control data. Thus, our results indicate that the HPA‐2 polymorphisms are not associated with an increased risk for AMI at early onset (< 46 years) both in men and in women.