Document Detail


Common polymorphisms of cyclooxygenase-2 and prostaglandin E2 receptor and increased risk for acute coronary syndrome in coronary artery disease.
MedLine Citation:
PMID:  18989535     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The arachidonic acid metabolites participate in development of coronary artery disease (CAD) and the plaque's instability. We assessed two common genetic polymorphisms: of cyclooxygenase-2 (COX-2) (COX2.8473, rs5275) and prostaglandin EP2 receptor gene (uS5, rs708494) in patients with CAD. Out of 1,368 patients screened by coronary arteriography, two groups fulfilled the entry criteria and were studied: stable coronary disease (sCAD, n = 125) and acute coronary syndromes (ACS, n = 63). They did not differ in the main characteristics. All patients were on aspirin at least seven days prior to the study. In 70 control subjects, the same genotypes were ascertained, expression of cyclooxygenases in peripheral blood monocytes was assessed by flow cytometry, and in-vitro biosynthesis of PGE(2) was measured by mass spectrometry. COX-2 CC homozygotes (variant allele), were more common, while EP2 GG homozygotes (wild-type) were less common in ACS (p = 0.03 and p = 0.017) than in the sCAD group. A combined genotype characterized by the presence of the wild-type COX2.8743T allele and the wild type homozygous EP2uS5 genotype (TT or CT | GG) decreased risk ratio of ACS in CAD patients (relative risk 0.41; 95% confidence interval 0.21-0.81). COX-2 polymorphism in control subjects did not affect the enzyme expression or PGE(2) production by peripheral blood monocytes, but production of PGE(2) increased by 40.1% in the subjects homozygous for EP2 receptor allele uS5A following lipopolysaccharide stimulation. In conclusion, the combined COX-2 (COX2.8473) and the EP2 receptor (uS5) genotypes seem to influence CAD stability, but in peripheral blood monocytes only EP2 receptor modulates PGE(2) production.
Authors:
Wojciech Szczeklik; Marek Sanak; Pawel Rostoff; Wieslawa Piwowarska; Bogdan Jakiela; Andrew Szczeklik
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Thrombosis and haemostasis     Volume:  100     ISSN:  0340-6245     ISO Abbreviation:  Thromb. Haemost.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-11-07     Completed Date:  2008-12-22     Revised Date:  2009-12-18    
Medline Journal Info:
Nlm Unique ID:  7608063     Medline TA:  Thromb Haemost     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  893-8     Citation Subset:  IM    
Affiliation:
Jagiellonian University, School of Medicine, Department of Medicine, ul. Skawinska 8, 31 - 066 Kraków, Poland.
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MeSH Terms
Descriptor/Qualifier:
Acute Coronary Syndrome / enzymology,  genetics*
Adult
Aged
Aged, 80 and over
Case-Control Studies
Coronary Artery Disease / complications,  enzymology,  genetics*
Cyclooxygenase 1 / metabolism
Cyclooxygenase 2 / genetics*,  metabolism
Dinoprostone / metabolism
Female
Gene Expression Regulation, Enzymologic*
Gene Frequency
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Monocytes / metabolism
Phenotype
Polymorphism, Genetic*
Prospective Studies
Receptors, Prostaglandin E / genetics*,  metabolism
Risk Assessment
Risk Factors
Chemical
Reg. No./Substance:
0/Receptors, Prostaglandin E; 0/prostaglandin EP2 receptor; 363-24-6/Dinoprostone; EC 1.14.99.1/Cyclooxygenase 1; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/PTGS1 protein, human; EC 1.14.99.1/PTGS2 protein, human

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