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. 2010 Jul;31(7):874-80.
doi: 10.1038/aps.2010.68. Epub 2010 Jun 28.

Exploring epistatic relationships of NO biosynthesis pathway genes in susceptibility to CHD

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Exploring epistatic relationships of NO biosynthesis pathway genes in susceptibility to CHD

Yuan-chao Tu et al. Acta Pharmacol Sin. 2010 Jul.

Abstract

Aim: To assess the epistatic relationships of nitric oxide (NO) biosynthesis pathway genes in susceptibility to coronary heart disease (CHD).

Methods: A total of 2142 subjects enrolled in two case-control studies was genotyped for 7 single-nucleotide polymorphisms (SNP) within NO biosynthesis pathway genes using TaqMan assays. The association analyses were performed at both SNP and haplotype levels. Two-way SNP-SNP interactions and high-order interactions were tested using multiple unconditional logistic regression analyses and generalized multifactor dimensionality reduction (GMDR) analyses, respectively.

Results: Two alleles (rs1049255*C and rs841*A) were identified that were significantly associated with increased risk of CHD after adjusting for all confounders (OR=1.21, 95% CI: 1.06-1.39, combined P=0.001, P(corr)=0.007 and OR=1.30, 95% CI 1.12-1.50, combined P<0.001, P(corr)<0.001, respectively). Significant two-way SNP-SNP interactions were found between SNP rs2297518 and these two significant polymorphisms, affecting the risk of CHD (P<0.001 for both). No significant high-order interactions were identified.

Conclusion: The results suggested that two-way SNP-SNP interactions of polymorphisms within NO biosynthesis pathway genes contribute to CHD risk.

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References

    1. Harrison DG. Cellular and molecular mechanisms of endothelial cell dysfunction. J Clin Invest. 1997;100:2153–7. - PMC - PubMed
    1. Moncada S, Higgs A. The L-arginine-nitric oxide pathway. N Engl J Med. 1993;329:2002–12. - PubMed
    1. Sessa WC. The nitric oxide synthase family of proteins. J Vasc Res. 1994;31:131–43. - PubMed
    1. Wang Y, Marsden PA. Nitric oxide synthases: Biochemical and molecular regulation. Curr Opin Nephrol Hypertens. 1995;4:12–2. - PubMed
    1. Esaki T, Hayashi T, Muto E, Yamada K, Kuzuya M, Iguchi A. Expression of inducible nitric oxide synthase in T lymphocytes and macrophages of cholesterol-fed rabbits. Atherosclerosis. 1997;128:39–46. - PubMed

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