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Soluble P‐selectin levels, P‐selectin polymorphisms and cardiovascular disease
Author(s) -
Carter A. M.,
Anagnostopoulou K.,
Mansfield M. W.,
Grant P. J.
Publication year - 2003
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1046/j.1538-7836.2003.00312.x
Subject(s) - p selectin , disease , l selectin , medicine , e selectin , immunology , genetics , biology , cell adhesion molecule , platelet , platelet activation , cell , cell adhesion
Summary.  P‐selectin is a member of the selectin family of cell adhesion molecules which are important in the transient attachment of leukocytes to endothelial cells and platelets. A number of polymorphisms in the gene encoding P‐selectin have been identified. Objectives were to investigate the relationship of soluble P (sP)‐selectin with P‐selectin gene polymorphisms and coronary artery disease (CAD). Two hundred and forty‐nine patients, with extent of CAD characterized by ≥50% stenosis in one or more coronary arteries, and 252 healthy controls were studied. Soluble P‐selectin was significantly higher in the patients than controls after adjustment for age, sex and smoking [patients 49.8 (47.5–52.1) ng mL −1 ; controls 46.7 (44.5–49.1) ng mL −1 , P  = 0.03). There was no association of sP‐selectin with myocardial infarction (MI) or presence of ≥50% stenosis. The −1817 T/C, −1969 G/A and −2123 C/G (but not the Thr715Pro) polymorphisms were in strong linkage disequilibrium. The Thr715Pro polymorphism was significantly associated with sP‐selectin even after adjustment for covariates [TT 48.9 (46.9–50.0) ng mL −1 ; TP + PP 40.7 (38.1–43.6) ng mL −1 , P  < 0.0001]. A significant interaction of Thr715Pro and smoking status was identified in the determination of sP‐selectin levels. There was no significant association of genotype at any of the polymorphism in relation to MI or stenosis. The Thr715Pro polymorphisms is associated with plasma sP‐selectin. This association is modulated by smoking, although the underlying mechanism remains unclear.

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