Making Sense of Epigenetics

Schuebel, Kornel E.; Gitik, Miri; Domschke, Katharina; Goldman, David

doi:10.1093/ijnp/pyw058

Cited by 63 publications

(39 citation statements)

References 89 publications

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“…Aside from histone modifications, alcohol can also modulate DNA methylation mechanisms in the brain (Schuebel et al, 2016). DNA methylation occurs when a methyl group from S-adenosyl methionine (SAM) is transferred to the cytosine residues in the dinucleotide sequence CpG.…”

Section: Epigenetic Mechanisms Of Alcohol Addictionmentioning

confidence: 99%

“…Genetic and environmental factors interact and appear to be equally important in the development of alcohol addiction (Schuebel et al, 2016; Starkman, Sakharkar, & Pandey, 2012). Stress and other psychiatric disorders, such as anxiety and mood disorders, can increase susceptibility to the development of alcohol use disorder (AUD; Figure 1); in fact, the presence of stress-related disorders leads subjects to consume alcohol in an attempt to attenuate the negative affective symptoms seen during addiction (Figure 1; Becker, 2012; Bolton, Robinson, & Sareen, 2009; Kushner, Abrams, & Borchardt, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…In particular, several studies report that neurobiological changes in the extended amygdala are critical for the interaction between alcohol addiction and stress-related disorders such as anxiety (Koob, 2008; Koob, & Volkow, 2010; Pandey, 2003; 2004). In fact, both stress and addiction can induce similar epigenetic modifications underlying changes in neurochemical pathways and synaptic plasticity in various structures of the extended amygdala suggesting a common link between alcoholism and stress-related disorders (Cadet, 2016; Moonat, & Pandey, 2012; Schuebel et al, 2016; Spanagel, Noori, & Heilig, 2014; Stamatakis et al, 2014). …”

Section: Introductionmentioning

confidence: 99%

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Epigenetic mechanisms of alcoholism and stress-related disorders

Palmisano

Pandey

2017

Alcohol

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Stress-related disorders, such as anxiety, early life stress and posttraumatic stress disorder appear to be important factors in promoting alcoholism, as alcohol consumption can temporarily attenuate the negative affective symptoms of these disorders. Several molecules involved in signaling pathways may contribute to the neuroadaptation induced during alcohol dependence and stress disorders, and among these, brain-derived neurotrophic factor (BDNF), corticotropin releasing factor (CRF), neuropeptide Y (NPY) and opioid peptides (i.e. nociceptin and dynorphin) are involved in the interaction of stress and alcohol. In fact, alterations in the expression and function of these molecules have been associated with the pathophysiology of stress-related disorders and alcoholism. In recent years, various studies have focused on the epigenetic mechanisms that regulate chromatin architecture thereby modifying gene expression. Interestingly, epigenetic modifications in specific brain regions have been shown to be associated with the neurobiology of psychiatric disorders, including alcoholism and stress. In particular, the enzymes responsible for chromatin remodeling (i.e. histone deacetylases and methyltransferases, DNA methyltransferases) have been identified as common molecular mechanisms for the interaction of stress and alcohol and have become promising therapeutic targets to treat or prevent alcoholism and associated emotional disorders.

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Section: Epigenetic Mechanisms Of Alcohol Addictionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Epigenetic mechanisms of alcoholism and stress-related disorders

Palmisano

Pandey

2017

Alcohol

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“…Thus these mechanisms are critical to developmental outcomes (Figure 1). Epigenetic events include the widely studied DNA methylation as well as histone modifications and non-coding RNA, mechanisms that are less widely explored [9]. In this review, we mainly consider the role of DNA methylation as a mechanism of plasticity in response to environmental exposures.…”

Section: Introductionmentioning

confidence: 99%

Environmentally Induced Epigenetic Plasticity in Development: Epigenetic Toxicity and Epigenetic Adaptation

Tian

Marsit

2018

Curr Epidemiol Rep

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Purpose of Review Epigenetic processes represent important mechanisms underlying developmental plasticity in response to environmental exposures. The current review discusses three classes of environmentally-induced epigenetic changes reflecting two aspects of that plasticity, toxicity effects as well as adaptation in the process of development. Recent findings Due to innate resilience, epigenetic changes caused by environmental exposures may not always lead impairments but may allow the organisms to achieve positive developmental outcomes through appropriate adaptation and a buffering response. Thus, some epigenetic adaptive responses to an immediate stimulus or exposure early in life would be expected to have a survival advantage but these same responses may also result in adverse developmental outcomes as they persists into later life stage. Although accumulating literature has identified environmentally induced epigenetic changes and linked them to health outcomes, we currently face challenges in the interpretation of the functional impact of their epigenetic plasticity. Summary Current environmental epigenetic research suggest that epigenetic processes may serve as a mechanism for resilience, and that they can be considered in terms of their impact on toxicity as a negative outcome, but also on adaptation for improved survival or health. This review encourages epigenetic environmental studies to move deeper inside into the functional meaning of epigenetic plasticity in the development.

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“…In general, the alcohol addiction cycle has been described as consisting of three stages: intoxication, withdrawal, and craving/abstinence (Koob and Volkow, 2010). Recently, the potential for involvement of changes in chromatin structure in alcohol abuse has been the focus of intensive research (Barbier et al, 2016; Finegersh et al, 2015; Gavin, Kusumo, Zhang, Guidotti, and Pandey, 2016; Mathies et al, 2015; Repunte-Canonigo et al, 2014; Schuebel, Gitik, Domschke, and Goldman, 2016). …”

Section: Introductionmentioning

confidence: 99%

Prefrontal cortex expression of chromatin modifier genes in male WSP and WSR mice changes across ethanol dependence, withdrawal, and abstinence

Hashimoto

Gavin

Wiren

et al. 2017

Alcohol

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Alcohol-use disorder (AUD) is a relapsing disorder associated with excessive ethanol consumption. Recent studies support the involvement of epigenetic mechanisms in the development of AUD. Studies carried out so far have focused on a few specific epigenetic modifications. The goal of this project was to investigate gene expression changes of epigenetic regulators that mediate a broad array of chromatin modifications after chronic alcohol exposure, chronic alcohol exposure followed by 8 h withdrawal, and chronic alcohol exposure followed by 21 days of abstinence in Withdrawal-Resistant (WSR) and Withdrawal Seizure-Prone (WSP) selected mouse lines. We found that chronic vapor exposure to highly intoxicating levels of ethanol alters the expression of several chromatin remodeling genes measured by quantitative PCR array analyses. The identified effects were independent of selected lines, which, however, displayed baseline differences in epigenetic gene expression. We reported dysregulation in the expression of genes involved in histone acetylation, deacetylation, lysine and arginine methylation and ubiquitination, and in DNA methylation during chronic ethanol exposure and withdrawal, but not after 21 days of abstinence. Ethanol-induced changes are consistent with decreased histone acetylation and with decreased deposition of the permissive ubiquitination mark H2BK120ub, associated with reduced transcription. On the other hand, ethanol-induced changes in the expression of genes involved in histone lysine methylation are consistent with increased transcription. The net result of these modifications on gene expression is likely to depend on the combination of the specific histone tail modifications present at a given time on a given promoter. Since alcohol does not modulate gene expression unidirectionally, it is not surprising that alcohol does not unidirectionally alter chromatin structure toward a closed or open state, as suggested by the results of this study.

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Making Sense of Epigenetics

Cited by 63 publications

References 89 publications

Epigenetic mechanisms of alcoholism and stress-related disorders

Epigenetic mechanisms of alcoholism and stress-related disorders

Environmentally Induced Epigenetic Plasticity in Development: Epigenetic Toxicity and Epigenetic Adaptation

Prefrontal cortex expression of chromatin modifier genes in male WSP and WSR mice changes across ethanol dependence, withdrawal, and abstinence

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