Investigation of an inducible nitric oxide synthase gene (NOS2A) polymorphism in a multiple sclerosis population

Tajouri, Lotti, Martin, Virginie, Ovcaric, Micky, Curtain, Rob P., Lea, Rod A., Csurhes, Peter, Pender, Michael P., & Griffiths, Lyn R. (2004) Investigation of an inducible nitric oxide synthase gene (NOS2A) polymorphism in a multiple sclerosis population. Brain Research Bulletin, 64(1), pp. 9-13.

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Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) affecting most commonly the Caucasian population. Nitric oxide (NO) is a biological signaling and effector molecule and is especially important during inflammation. Inducible nitric oxide synthase (iNOS) is one of the three enzymes responsible for generating NO. It has been reported that there is an excessive production of NO in MS concordant with an increased expression of iNOS in MS lesions. This study investigated the role of a bi-allelic tetranucleotide polymorphism located in the promoter region of the human iNOS (NOS2A) gene in MS susceptibility. A group of MS patients (n = 101) were genotyped and compared to an age- and sex-matched group of healthy controls (n = 101). The MS group was subdivided into three subtypes, namely relapsing-remitting MS (RR-MS), secondary-progressive MS (SP-MS) and primary-progressive MS (PP-MS). Results of a chi-squared analysis and a Fisher's exact test revealed that allele and genotype distributions between cases and controls were not significantly different for the total population (chi(2) = 3.4, P(genotype) = 0.15; chi(2) = 3.4, P(allele) = 0.082) and for each subtype of MS (P > 0.05). This suggests that there is no direct association of this iNOS gene variant with MS susceptibility.

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ID Code: 62744
Item Type: Journal Article
Refereed: Yes
DOI: 10.1016/j.brainresbull.2004.04.019
ISSN: 0361-9230
Divisions: Current > Institutes > Institute of Health and Biomedical Innovation
Copyright Owner: Copyright 2004 Elsevier Inc.
Deposited On: 20 Sep 2013 05:00
Last Modified: 02 Jul 2014 23:03

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