Effect of long-term mental and pain stress on the dynamics of H4 histone acetylation in hippocampal neurons of rats with different levels of nervous system excitability

Соколова, Н. Е.; Shiryaeva, N. V.; Dyuzhikova, N. A.; Savenko, Yu. N.; Vaido, A. I.

doi:10.1007/s10517-006-0361-3

Cited by 11 publications

(4 citation statements)

References 2 publications

(1 reference statement)

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“…Histone modifications have been implicated in broad neurobiological processes such as development of the CNS (reviewed in MacDonald and Roskams, 2009), post-traumatic stress disorders (Sokolova et al, 2006), childhood abuse/suicide (Meaney et al, 2007; McGowan et al, 2009), memory formation (Gupta et al, 2010), and addiction (Impey, 2007); specific physiologic processes such as neuronal differentiation (Kular et al, 2009), regulation of choline acetyltransferase activity (Aizawa and Yamamuro, 2010), astrocyte GDNF and BDNF transcription (Wu et al, 2008), microglial apoptosis (Chen et al, 2007), and axon pathfinding (Zinovyeva et al, 2006); and various neurologic disorders, including Parkinson’s disease (Chen et al, 2007; Wu et al, 2008), motor neuron disease (reviewed in Echaniz-Laguna et al, 2008), multiple sclerosis (reviewed in Gray and Dangond, 2006), X-linked mental retardation (Tahiliani et al, 2007), and stroke/cerebral palsy (Meisel et al, 2006). All of these histone-related processes occur in the context of the CNS, and many have been reported to function as dynamic regulatory mechanisms in postmitotic neurons.…”

Section: 0 Dynamic Epigenetic Regulation In Adult Neuronsmentioning

confidence: 99%

Epigenetic mechanisms in Alzheimer's disease

Mastroeni

Grover

Delvaux

et al. 2011

Neurobiology of Aging

226

162

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Epigenetic modifications help orchestrate sweeping developmental, aging, and disease-causing changes in phenotype by altering transcriptional activity in multiple genes spanning multiple biologic pathways. Although previous epigenetic research has focused primarily on dividing cells, particularly in cancer, recent studies have shown rapid, dynamic, and persistent epigenetic modifications in neurons that have significant neuroendocrine, neurophysiologic, and neurodegenerative consequences. Here, we provide a review of the major mechanisms for epigenetic modification and how they are reportedly altered in aging and Alzheimer’s disease (AD). Because of their reach across the genome, epigenetic mechanisms may provide a unique integrative framework for the pathologic diversity and complexity of AD.

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Section: 0 Dynamic Epigenetic Regulation In Adult Neuronsmentioning

confidence: 99%

Epigenetic mechanisms in Alzheimer's disease

Mastroeni

Grover

Delvaux

et al. 2011

Neurobiology of Aging

226

162

View full text Add to dashboard Cite

show abstract

“…The HC is particularly susceptible to structural, functional, and neurogenic rearrangements in response to environmental stimuli [13][14][15]. Several research groups have reported evidence that these alterations are regulated by epigenetic processes, defined as inheritable states of gene activity not based on changes in DNA sequence [16][17][18]. One of the major epigenetic mechanisms is DNA cytosine methylation [19].…”

Section: Introductionmentioning

confidence: 99%

Vitamin B12 is neuroprotective in experimental pneumococcal meningitis through modulation of hippocampal DNA methylation

Queiroz

Cavalcante-Silva

Lopes

et al. 2020

J Neuroinflammation

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Background Bacterial meningitis (BM) causes apoptotic damage to the hippocampus and homocysteine (Hcy) accumulation to neurotoxic levels in the cerebrospinal fluid of children. The Hcy pathway controls bioavailability of methyl, and its homeostasis can be modulated by vitamin B12, a cofactor of the methionine synthase enzyme. Herein, the neuroprotective potential and the underlying mode of action of vitamin B12 adjuvant therapy were assessed in an infant rat model of BM. Methods Eleven-day old rats were intracysternally infected with Streptococcus pneumoniae serotype 3, or saline, treated with B12 or placebo, and, 24 h after infection, their hippocampi were analyzed for apoptosis in the dentate gyrus, sulfur amino acids content, global DNA methylation, transcription, and proximal promoter methylation of candidate genes. Differences between groups were compared using 2-way ANOVA followed by Bonferroni post hoc test. Correlations were tested with Spearman’s test. Results B12 attenuated BM-induced hippocampal apoptosis in a Hcy-dependent manner (r = 0.80, P < 0.05). BM caused global DNA hypomethylation; however, B12 restored this parameter. Accordingly, B12 increased the methylation capacity of hippocampal cells from infected animals, as inferred from the ratio S-adenosylmethionine (SAM):S-adenosylhomocysteine (SAH) in infected animals. BM upregulated selected pro-inflammatory genes, and this effect was counteracted by B12, which also increased methylation of CpGs at the promoter of Ccl3 of infected animals. Conclusion Hcy is likely to play a central role in hippocampal damage in the infant rat model of BM, and B12 shows an anti-inflammatory and neuroprotective action through methyl-dependent epigenetic mechanisms.

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“…In the hippocampus, evidence that histone modifications might play a significant role in the function of the structure came from the work of Weaver (11), who showed that differences in maternal behavior produced differences in the behavior of offspring, and that this difference was associated with changes in histone acetylation, and could be blocked by a histone deacetylase inhibitor. Subsequent work has connected acetylation of histone H4 (12) and acetylation, phosphorylation and methylation of H3 in the hippocampus with stress (13)(14)(15). Histone lysine methylation, unlike acetylation, for example, is remarkable for the site specificity of its associated machinery and its ability to recruit specific effector protein complexes (16)(17)(18).…”

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confidence: 99%

Regulation of hippocampal H3 histone methylation by acute and chronic stress

Hunter

McCarthy²,

Milne³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

261

190

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The hippocampal formation is a brain region noted for its plasticity in response to stressful events and adrenal steroid hormones. Recent work has shown that chromatin remodeling in various brain regions, including the hippocampus, is associated with the effects of stress in a variety of models. We chose to examine the effects of stress, stress duration, corticosterone administration, and fluoxetine treatment on the levels of hippocampal histone H3 methylation at lysines 4, 9, and 27, marks associated, respectively, with active transcription, heterochromatin formation, and transcriptional repression. We found that acute stress increased the levels of H3K9 tri-methylation (H3K9me3) in the dentate gyrus (DG) and CA1, while it reduced levels of H3K9 mono-methylation (H3K9me1) and H3K27 tri-methylation (H3K27me3) in the same regions, and had no effect on levels of H3K4 tri-methylation (H3K4me3). Seven days of restraint stress reduced levels of H3K4me3 in the CA1 and H3K27me3 in the DG and CA1, while increasing basal levels of H3K9me3. Chronic restraint stress (CRS) for 21 days mildly increased levels of H3K4me3 and reduced H3K9me3 levels in the DG. Treatment with fluoxetine during CRS reversed the decrease in DG H3K9me3, but had no effect on the other marks. These results show a complex, surprisingly rapid, and regionally specific pattern of chromatin remodeling within hippocampus produced by stress and anti-depressant treatment that may open an avenue of understanding the interplay of stress and hippocampal gene expression, and reveal the outlines of a potential chromatin stress response that may be diminished or degraded by chronic stress.brain ͉ chromatin ͉ corticosteroids ͉ fluoxetine

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Effect of long-term mental and pain stress on the dynamics of H4 histone acetylation in hippocampal neurons of rats with different levels of nervous system excitability

Cited by 11 publications

References 2 publications

Epigenetic mechanisms in Alzheimer's disease

Epigenetic mechanisms in Alzheimer's disease

Vitamin B12 is neuroprotective in experimental pneumococcal meningitis through modulation of hippocampal DNA methylation

Regulation of hippocampal H3 histone methylation by acute and chronic stress

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