Citation

Gross JA, Fiori LM, Labonté B, Lopez JP, Turecki G. J. Psychiatr. Res. 2013; 47(4): 513-519.

Affiliation

McGill Group for Suicide Studies, Douglas Mental Health University Institute, McGill University, 6875 boul. Lasalle, Verdun, Quebec H4H 1R3, Canada.

Copyright

(Copyright © 2013, Elsevier Publishing)

DOI

10.1016/j.jpsychires.2012.11.016

PMID

23260169

Abstract

Suicide is among the leading causes of death worldwide. The polyamine system has been increasingly implicated in the neurobiology of suicide. Previous research has indicated that epigenetic mechanisms play a role in explaining dysregulation of polyamine genes in suicide completers. Nevertheless, regulatory mechanisms explaining polyamine biosynthetic genes displaying dysregulated expression in suicide completers, including ornithine decarboxylase antizymes 1 and 2 (OAZ1 and OAZ2), S-adenosylmethionine decarboxylase (AMD1), and arginase 2 (ARG2), have yet to be elucidated. In this study, we investigated methylation patterns in the promoter region of OAZ1, OAZ2, AMD1, and ARG2 in Brodmann area 44 from a group of 33 suicide completers and 31 non-suicide controls. We found significant site-specific differences in methylation in the promoter of ARG2 and AMD1 that were also significantly negatively correlated with gene expression. These findings provide further support for a role for the involvement of epigenetic modifications in the regulation of genes associated with polyamine biosynthesis, and which may contribute to the complexity of suicidal behaviors.

Language: en