Lack of association between endothelial nitric oxide synthase (NOS3) gene polymorphisms and suicide attempts.

Pilar A Sáiz,Blanca Morales,Celso Arango,Julio Bobes,Manuel Bousoño,Teresa Bascarán,Victoria Alvarez,Eliecer Coto,Maria P García-Portilla,Begoña Paredes

doi:10.1186/1744-9081-3-32

Abstract

ObjectiveThe aim of this study is to investigate the association between two polymorphisms of endothelial nitric oxide synthase (NOS3) and suicide attempts.MethodsWe genotyped 186 suicide attempters and 420 unrelated healthy controls. The following polymorphisms were analysed: T-786C and 27-bp repeat in intron 4.ResultsNo significant differences were found in genotype or in allelic distribution of the aforesaid polymorphisms. There were also no differences in the genotype distribution or allelic frequencies when separately assessing males and females or impulsive and non-impulsive attempters and normal controls. Estimated haplotype frequencies were similar in both groups.ConclusionOur data do not support the hypothesis that genetically determined changes in the NOS3 gene confer increased susceptibility for suicidal behavior.

Highlights

Called endothelial NOS, or eNOS) is the predominant isoform in most tissues [3]
Behavioral and Brain Functions 2007, 3:32 http://www.behavioralandbrainfunctions.com/content/3/1/32 otide polymorphism (SNP), T-786C, and a 27-bp repeat in intron 4) result in a reduction in NOS3 gene promoter activity [7] and function as an epistatic enhancer element depending on T-786C genotype [8], respectively
No association between NOS3 gene polymorphisms and suicidal behavior was found in our sample

Summary

Introduction

Called endothelial NOS, or eNOS) is the predominant isoform in most tissues [3]. NOS3 is involved in the proliferation of neuronal progenitor cells, which might be implicated in the pathophysiology of depressive disorders [4,5]. Behavioral and Brain Functions 2007, 3:32 http://www.behavioralandbrainfunctions.com/content/3/1/32 otide polymorphism (SNP), T-786C (rs2070744), and a 27-bp repeat in intron 4) result in a reduction in NOS3 gene promoter activity [7] and function as an epistatic enhancer element depending on T-786C genotype [8], respectively. We hypothesized that two functional genetic variants of the NOS3 gene

Results

Conclusion