| Common polymorphisms of cyclooxygenase-2 and prostaglandin E2 receptor and increased risk for acute coronary syndrome in coronary artery disease. | |
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MedLine Citation:
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PMID: 18989535 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Wojciech Szczeklik; Marek Sanak; Pawel Rostoff; Wieslawa Piwowarska; Bogdan Jakiela; Andrew Szczeklik |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Thrombosis and haemostasis Volume: 100 ISSN: 0340-6245 ISO Abbreviation: Thromb. Haemost. Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-11-07 Completed Date: 2008-12-22 Revised Date: 2009-12-18 |
Medline Journal Info:
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Nlm Unique ID: 7608063 Medline TA: Thromb Haemost Country: Germany |
Other Details:
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Languages: eng Pagination: 893-8 Citation Subset: IM |
Affiliation:
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Jagiellonian University, School of Medicine, Department of Medicine, ul. Skawinska 8, 31 - 066 Kraków, Poland. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Coronary Syndrome
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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:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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