The pro-inflammatory cytokine LTA (lymphotoxin-α) has multiple functions in regulating the immune system and may contribute to inflammatory processes leading to CHD (coronary heart disease). The aim of the present study was to investigate whether the common C804A (resulting in a Thr26→Asp amino acid substitution) and A252G polymorphisms of the LTA gene and the C3279T polymorphism of the galectin-2 (LGALS2) gene, which affects LTA secretion, are associated with inflammatory parameters and cell adhesion molecules, and whether these polymorphisms are related to CHD in American women and men. We conducted a prospective nested case-control study within the Nurses' Health Study and Health Professionals Follow-Up Study. Among participants free of cardiovascular disease at baseline, 249 women and 266 men developed CHD during 8 and 6 years of follow-up respectively, and we matched controls 2:1 based on age and smoking. The LGALS2 gene variant was significantly associated with a decreased risk of CHD in women [odds ratio (95% confidence interval), 0.70 (0.50–0.97); P=0.03]. In addition, the LGALS2 polymorphism was directly associated with CRP (C-reactive protein) levels in cases from both studies (P<0.05). The LTA gene polymorphisms were directly associated with levels of sTNFRs (soluble tumour necrosis factor receptors) and VCAM-1 (vascular cell adhesion molecule-1) in both women and men with CHD (P<0.05). However, no overall effect was demonstrated between LTA gene polymorphisms and risk of CHD.
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March 2007
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Research Article|
February 01 2007
Effects of lymphotoxin-α gene and galectin-2 gene polymorphisms on inflammatory biomarkers, cellular adhesion molecules and risk of coronary heart disease
Folkert W. Asselbergs;
*Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, U.S.A.
†Department of Cardiology, University Medical Center Groningen, P.O. Box 30001, Hanzeplein 1, 9700 RB, Groningen, The Netherlands
Correspondence: Dr Folkert W. Asselbergs (email [email protected]).
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Jennifer K. Pai;
Jennifer K. Pai
‡Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, U.S.A.
§Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, U.S.A.
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Kathryn M. Rexrode;
Kathryn M. Rexrode
∥Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, 900 Commonwealth Avenue, Boston, MA 02115, U.S.A.
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David J. Hunter;
David J. Hunter
*Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, U.S.A.
‡Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, U.S.A.
§Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, U.S.A.
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Eric B. Rimm
Eric B. Rimm
*Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, U.S.A.
‡Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, U.S.A.
§Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, U.S.A.
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Publisher: Portland Press Ltd
Received:
July 26 2006
Revision Received:
September 27 2006
Accepted:
October 16 2006
Accepted Manuscript online:
October 16 2006
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society
2007
Clin Sci (Lond) (2007) 112 (5): 291–298.
Article history
Received:
July 26 2006
Revision Received:
September 27 2006
Accepted:
October 16 2006
Accepted Manuscript online:
October 16 2006
Citation
Folkert W. Asselbergs, Jennifer K. Pai, Kathryn M. Rexrode, David J. Hunter, Eric B. Rimm; Effects of lymphotoxin-α gene and galectin-2 gene polymorphisms on inflammatory biomarkers, cellular adhesion molecules and risk of coronary heart disease. Clin Sci (Lond) 1 March 2007; 112 (5): 291–298. doi: https://doi.org/10.1042/CS20060200
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