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Sun, F., Akazawa, S., Sugahara, K., Kamihira, S., Kawasaki, E., Eguchi, K. and Koji, T. (2002) Apoptosis in Normal Rat Embryo Tissues during Early Organogenesis: The Possible Involvement of Bax and Bcl-2. Archives of Histology and Cytology, 65, 145-157.
https://doi.org/10.1679/aohc.65.145

has been cited by the following article:

• TITLE: Association of Bax and Bcl-2 Functional Polymorphisms and Protein Levels with Posttraumatic Stress Disorder

  AUTHORS: Diana Avetyan, Arsen Arakelyan, Gohar Mkrtchyan

  KEYWORDS: Posttraumatic Stress Disorder, Apoptosis, BCL2, BAX, Single Nucleotide Polymorphisms

  JOURNAL NAME: Journal of Biosciences and Medicines, Vol.6 No.2, February 26, 2018

  ABSTRACT: Background: Posttraumatic stress disorder (PTSD) is an anxiety disease influenced by both environmental and genetic factors, which affects a patient’s quality of life and social stability. Recent studies have shown that the pathogenesis of PTSD is associated with apoptosis; however, the molecular mechanisms that cause such damage are not well-understood. Also it is unclear whether these pathologic alterations are genetically determined or caused by other factors. The aim of this study was to investigate the genetic association of functional polymorphisms in genes coding for apoptosis-related Bcl-2 and Bax proteins with PTSD as well as proteins levels in the blood of affected subjects. Methods: The study groups consisted of 200 combat veterans with PTSD and an equal number of healthy subjects with no family- or past-history of any psychiatric disorders. Bax and Bcl-2 proteins levels in blood were measured by ELISA. DNA samples were genotyped for SNPs using PCR-SSP. Results: According to our results, PTSD patients are characterized by increased levels of apoptotic proteins and the imbalance in the Bax/Bcl-2 ratio compared to healthy subjects. Our results also demonstrate that rs956572*A minor allele of the BCL2 gene was overrepresented in patients with PTSD compared to healthy subjects. Conclusions: The results implicate Bcl-2 and Bax in pathogenesis of PTSD on genetic and protein levels, though further studies on enlarged cohort and in different populations are required.