COX-2 Gene Promoter Polymorphism and Coronary Artery Disease in Middle-Aged Men: The Helsinki Sudden Death Study

Cyclooxygenase (COX) catalyzes formation of prostaglandins that contribute to the inflammation in atherosclerosis. Our objective was to study whether the functional C variant of the −765G→C polymorphism in the human COX-2 gene associates with the severity of coronary atherosclerosis measured at the...

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Main Authors: Kati H. Huuskonen, Tarja A. Kunnas, Minna M. Tanner, Jussi Mikkelsson, Erkki Ilveskoski, Pekka J. Karhunen, Seppo T. Nikkari
Format: Article
Language:English
Published: Wiley 2008-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2008/289453
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author Kati H. Huuskonen
Tarja A. Kunnas
Minna M. Tanner
Jussi Mikkelsson
Erkki Ilveskoski
Pekka J. Karhunen
Seppo T. Nikkari
author_facet Kati H. Huuskonen
Tarja A. Kunnas
Minna M. Tanner
Jussi Mikkelsson
Erkki Ilveskoski
Pekka J. Karhunen
Seppo T. Nikkari
author_sort Kati H. Huuskonen
collection DOAJ
description Cyclooxygenase (COX) catalyzes formation of prostaglandins that contribute to the inflammation in atherosclerosis. Our objective was to study whether the functional C variant of the −765G→C polymorphism in the human COX-2 gene associates with the severity of coronary atherosclerosis measured at the coronary artery level. The Helsinki sudden death study autopsy material (n = 300) comprised of Finnish men who died suddenly. The area of atherosclerotic lesions in the coronary arteries was quantitated, and coronary narrowing was measured. The occurrence of myocardial infarction (MI) was assessed. Genotyping was by restriction endonuclease analysis. Men carrying the minor C allele had larger areas of complicated lesions (P = .024) and a higher number of coronary arteries that had over 50% stenosis (P = .036) compared to men representing the common GG genotype. The COX-2 polymorphism was not associated with MI. Our data suggest that COX-2 may be involved in plaque growth.
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institution Kabale University
issn 0962-9351
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language English
publishDate 2008-01-01
publisher Wiley
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series Mediators of Inflammation
spelling doaj-art-1f007c155a48414ebced52032baf540a2025-02-03T01:07:31ZengWileyMediators of Inflammation0962-93511466-18612008-01-01200810.1155/2008/289453289453COX-2 Gene Promoter Polymorphism and Coronary Artery Disease in Middle-Aged Men: The Helsinki Sudden Death StudyKati H. Huuskonen0Tarja A. Kunnas1Minna M. Tanner2Jussi Mikkelsson3Erkki Ilveskoski4Pekka J. Karhunen5Seppo T. Nikkari6Department of Medical Biochemistry, Medical School, University of Tampere, Tampere 33104, FinlandDepartment of Medical Biochemistry, Medical School, University of Tampere, Tampere 33104, FinlandLaboratory of Cancer Genetics, Institute of Medical Technology, University of Tampere, Tampere 33104, FinlandDepartment of Forensic Medicine, Medical School, University of Tampere, Tampere 33104, FinlandDepartment of Forensic Medicine, Medical School, University of Tampere, Tampere 33104, FinlandDepartment of Forensic Medicine, Medical School, University of Tampere, Tampere 33104, FinlandDepartment of Medical Biochemistry, Medical School, University of Tampere, Tampere 33104, FinlandCyclooxygenase (COX) catalyzes formation of prostaglandins that contribute to the inflammation in atherosclerosis. Our objective was to study whether the functional C variant of the −765G→C polymorphism in the human COX-2 gene associates with the severity of coronary atherosclerosis measured at the coronary artery level. The Helsinki sudden death study autopsy material (n = 300) comprised of Finnish men who died suddenly. The area of atherosclerotic lesions in the coronary arteries was quantitated, and coronary narrowing was measured. The occurrence of myocardial infarction (MI) was assessed. Genotyping was by restriction endonuclease analysis. Men carrying the minor C allele had larger areas of complicated lesions (P = .024) and a higher number of coronary arteries that had over 50% stenosis (P = .036) compared to men representing the common GG genotype. The COX-2 polymorphism was not associated with MI. Our data suggest that COX-2 may be involved in plaque growth.http://dx.doi.org/10.1155/2008/289453
spellingShingle Kati H. Huuskonen
Tarja A. Kunnas
Minna M. Tanner
Jussi Mikkelsson
Erkki Ilveskoski
Pekka J. Karhunen
Seppo T. Nikkari
COX-2 Gene Promoter Polymorphism and Coronary Artery Disease in Middle-Aged Men: The Helsinki Sudden Death Study
Mediators of Inflammation
title COX-2 Gene Promoter Polymorphism and Coronary Artery Disease in Middle-Aged Men: The Helsinki Sudden Death Study
title_full COX-2 Gene Promoter Polymorphism and Coronary Artery Disease in Middle-Aged Men: The Helsinki Sudden Death Study
title_fullStr COX-2 Gene Promoter Polymorphism and Coronary Artery Disease in Middle-Aged Men: The Helsinki Sudden Death Study
title_full_unstemmed COX-2 Gene Promoter Polymorphism and Coronary Artery Disease in Middle-Aged Men: The Helsinki Sudden Death Study
title_short COX-2 Gene Promoter Polymorphism and Coronary Artery Disease in Middle-Aged Men: The Helsinki Sudden Death Study
title_sort cox 2 gene promoter polymorphism and coronary artery disease in middle aged men the helsinki sudden death study
url http://dx.doi.org/10.1155/2008/289453
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