2007
DOI: 10.1016/j.pnpbp.2006.12.014
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Altered HDAC5 and CREB mRNA expressions in the peripheral leukocytes of major depression

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Cited by 90 publications
(70 citation statements)
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“…The induction of HDACs 2/5 and 4 in unipolar and bipolar patients, respectively, only in the depressive state suggests that these changes may be associated with depression symptoms rather than adaptive responses, and agree with the general consensus (albeit with some exceptions) that histone acetylation in brain has a pro-adaptive role in stress and depression. Further concurring with the pro-depressive role of HDAC5 in the hippocampus, another study found that peripheral expression of HDAC5 was higher in drug-free depressive patients compared with controls, with this effect reversed after chronic antidepressant treatment (Iga et al, 2007). Although the study of sirtuins in depression is largely lacking, one study found that SIRTs 1, 2, and 6 are decreased in both MDD and bipolar patients in the depressive state but not remitted state.…”
Section: Reviewmentioning
confidence: 81%
“…The induction of HDACs 2/5 and 4 in unipolar and bipolar patients, respectively, only in the depressive state suggests that these changes may be associated with depression symptoms rather than adaptive responses, and agree with the general consensus (albeit with some exceptions) that histone acetylation in brain has a pro-adaptive role in stress and depression. Further concurring with the pro-depressive role of HDAC5 in the hippocampus, another study found that peripheral expression of HDAC5 was higher in drug-free depressive patients compared with controls, with this effect reversed after chronic antidepressant treatment (Iga et al, 2007). Although the study of sirtuins in depression is largely lacking, one study found that SIRTs 1, 2, and 6 are decreased in both MDD and bipolar patients in the depressive state but not remitted state.…”
Section: Reviewmentioning
confidence: 81%
“…Alterations in the acetylation pattern of lysine residues comprising amino acid tails of histones 3 ( Fig. 2C) and 4 have been implicated in depression (Iga et al, 2007;Levine et al, 2012;Onishchenko et al, 2008;Tsankova et al, 2006) and antidepressant treatment (Belzeaux et al, 2012;Dyrvig et al, 2012;Tsankova et al, 2006Tsankova et al, , 2004.…”
Section: Histone Acetylation and Methylationmentioning
confidence: 98%
“…Tissue Diagnosis Epigenetic modification, molecular changes and other outcomes Cruceanu et al (2013) Prefrontal cortex (BA 10) MDD or BP ↑H3K4 methylation at SYN1 promoter in MDD ↑mRNA for SYN1a in BP and MDD ↑mRNA for SYN1b in MDD only ↑H3K4 methylation at SYN2 promoter in BP ↑mRNA for SYN2a in BP and ↑mRNA for SYN2b in MDD Ernst et al (2009a), Ernst et al (2009b) Frontal cortex Suicide completers, some of whom had MDD ↑DNA and H3K27 methylation of Trk B-T1 ↓Trk B-T1 mRNA Fuchikami et al (2011) Blood MDD Altered BDNF DNA methylation pattern in MDD He et al (2012) Blood MDD SNPs in microRNA processing genes in DGCR8 and AGO1 DGCR8 SNP associated with ↑suicide risk and improved antidepressant response and AGO1 SNP associated with ↓suicide risk Iga et al (2007) Blood MDD ↑HDAC 5 mRNA Keller et al (2011), Keller et al (2010 Wernicke's area Suicide completers, some of whom had MDD ↑DNA methylation and ↓mRNA for BDNF but no correlation between Trk B and Trk B-T1 DNA methylation and suicide Philibert et al (2008) Lymphoblast cell lines MDD Females showed higher levels of DNA methylation of SERT compared to males Trend for association between ↑SERT DNA methylation and MDD Poulter et al (2008) Frontal cortex Suicide completers with MDD ↑DNA methylation of GABA A receptor subunit α1 Rahman et al (2010) Buccal epithelial cells MDD or BP Association between a polymorphism in P2X7 purinergic receptor gene and target site for miR-625 and -1302 Saus et al (2010) Blood MDD Association between a polymorphism in the circadian clock modulator pre-miR-182 and late insomnia Smalheiser et al (2012) Prefrontal cortex (BA 9)…”
Section: Referencementioning
confidence: 99%
“…A still limited number of studies have reported alterations of class IIa HDACs in several cancers (Chaabouni et al, 2006;Ouaissi et al, 2008;Ozdag et al, 2006;Yuki et al, 2004) and neuronal disorders (Hoshino et al, 2003;Iga et al, 2007;Renthal et al, 2007). Armed with the new insights into their regulation and biological functions, it seems possible to specifically modulate class IIa HDAC activity and normalize pathological gene expression patterns in disorders such as cardiac hypertrophy, hearth failure, tumour growth or skeletal muscle wasting.…”
Section: Future Prospectsmentioning
confidence: 99%