Association study of EP1 gene polymorphisms with suicide completers in the Japanese population

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Abstract

Background: Both environmental and genetic factors have been reported to be involved in suicidal behaviors. Considerable evidence indicates that impulsive aggression is one of the important risk factors that contribute to suicide. A recent study has shown that prostaglandin E2 type 1 receptor (EP1) signaling regulates impulsive-aggressive behaviors in mice under both social and environmental stresses. To test the possible involvement of the EP1 gene in suicide, we carried out an association study of EP1 gene polymorphisms with suicide completers in the Japanese population. Methods: We studied 5 SNPs including one SNP in exon 2 (rs3745459) and four SNPs in the potential promoter region of the EP1 gene (rs3810255, rs3810254, rs3810253 and rs10416814) in 374 healthy control and 287 completed suicide victims using standard Taqman probe genotyping assays. Results: No significant differences of the genotypic distribution, allelic frequency or haplotype distribution between controls and suicide completers were found. Gender based analysis revealed that genotypic, allelic and haplotypic distributions of rs3810255, rs3810254, rs3810253 and rs10416814 SNPs were significantly different between the female control and female suicide groups, although the differences did not withstand correction for multiple comparisons. Conclusion: We could not find an association of EP1 gene with suicide in the Japanese population. Because several SNPs in the promoter region of the EP1 gene were nominally significantly associated with suicide in the female, further studies with a larger sample size and different population are needed to confirm this result. © 2011 Elsevier Inc.

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Cui, H., Supriyanto, I., Sasada, T., Shiroiwa, K., Fukutake, M., Shirakawa, O., … Hishimoto, A. (2011). Association study of EP1 gene polymorphisms with suicide completers in the Japanese population. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 35(4), 1108–1111. https://doi.org/10.1016/j.pnpbp.2011.03.010

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