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Chie Nishioka performed all experiments and wrote the article.Atsuya Nobumoto and Masayuki Tsuda provided technical support.Alterations in m RNA expression of apoptosis-related genes BCL2, BAX, FAS, caspase-3, and the novel member BCL2L12 after treatment of human leukemic cell line HL60 with the antineoplastic agent etoposide Two acute monocytic leukemia (AML-M5a) cell lines (MOLM-13 and MOLM-14) with interclonal phenotypic heterogeneity showing MLL-AF9 fusion resulting from an occult chromosome insertion, ins(11;9)(q23;p22p23)This work was supported in part by Takeda Science Foundation (to CN) and JSPS KAKENHI Grant Number 14446690 (to CN).Author contributions Takayuki Ikezoe contributed to the concept and design, interpreted and analyzed the data and wrote the article.* Denotes the two studies (Perroud et al., 2014b and Martin-Blanco et al., 2014) that were included twice in this overview because they contained site-specific methylation data based on both adverse life experiences and adversity-related conditions. doi: 10.1017/S1461145713000102 Pubmed Abstract | Pubmed Full Text | Cross Ref Full Text | Google Scholar Moore, L. Heightened promoter methylation is typically associated with downregulation of gene expression, whereas intragenic methylation correlates with higher transcriptional activity (Jones, 2012; Moore et al., 2013; Yang et al., 2014). Western blot analysis indicated that BCL2L12 was aberrantly expressed in patient-isolated AML cells and AML cell lines.Furthermore, CD82 blockade by a specific antibody downregulated BCL2L12 in parallel with dephosphorylation of signal transducer and activator of transcription 5 (STAT5) and AKT, whereas pharmacological inhibition of STAT5 and AKT activation decreased BCL2L12 expression in leukemia cells.
Studies attempting to understand stress-dependent developmental programming, have largely focused on promoter methylation of stress-regulatory genes, such as the glucocorticoid receptor (GR) gene, in association with vulnerability and resilience to psychiatric disorders (Daskalakis et al., 2013). doi: 10.1002/cam4.22 Pubmed Abstract | Pubmed Full Text | Cross Ref Full Text | Google Scholar Palosaari, E., Punamaki, R.
Many studies focused on methylation of the glucocorticoid receptor exon 1F promoter following an initial observation that changes in this region could be modulated by the environment. doi: 10.3109/15622975.2013.866693 Pubmed Abstract | Pubmed Full Text | Cross Ref Full Text | Google Scholar Perroud, N., Salzmann, A., Prada, P., Nicastro, R., Hoeppli, M.
This review examines all published studies that have attempted to measure methylation in this region using different techniques, several tissue types, populations at different behavioral state and stages of development.
More studies examined methylation in this region (Moser et al., 2007; Alt et al., 2010; Radtke et al., 2011; Mulligan et al., 2012; Steiger et al., 2013; Yehuda et al., 2013, 2014a; Rodney and Mulligan, 2014), but only the above 16 report methylation differences at a single Cp G site resolution. Methylation changes at NR3C1 in newborns associate with maternal prenatal stress exposure and newborn birth weight. doi: 10.4161/epi.21180 Pubmed Abstract | Pubmed Full Text | Cross Ref Full Text | Google Scholar Na, K.
It is already becoming clear that different studies use different methodologies, examine slightly different sub-regions, and accordingly, produce different findings with respect to directionality of the associations with stressful experience and stress-related illness (Figure 2).