ArticleHepatology international2014
Epigenetic histone modifications in a clinically relevant rat model of chronic ethanol-binge-mediated liver injury.
Article in Hepatology international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Nascent liver proteome reveals enzymes and transcription regulators under physiological and alcohol exposure conditions.Nature communications · 2025Article
- Regional and temporal dynamics of DNA methylation and epigenetic gene regulation in response to binge-like alcohol exposure in the adolescent mouse brain.Frontiers in molecular neuroscience · 2025Article
- Proteomic analysis of alcohol-associated hepatitis reveals glycoprotein NMB (GPNMB) as a novel hepatic and serum biomarker.Alcohol (Fayetteville, N.Y.) · 2022Article
- miR-4286 functions in osteogenesis and angiogenesis via targeting histone deacetylase 3 and alleviates alcohol-induced bone loss in mice.Cell proliferation · 2021Article
- Hepatic COX-2 expression protects mice from an alcohol-high fat diet-induced metabolic disorder by involving protein acetylation related energy metabolism.Alcohol (Fayetteville, N.Y.) · 2021Article
- Binge Alcohol Is More Injurious to Liver in Female than in Male Rats: Histopathological, Pharmacologic, and Epigenetic Profiles.The Journal of pharmacology and experimental therapeutics · 2019Article
- Review
- Animal Models of Alcoholic Liver Disease: Pathogenesis and Clinical Relevance.Gene expression · 2017Review
- Binge alcohol alters PNPLA3 levels in liver through epigenetic mechanism involving histone H3 acetylation.Alcohol (Fayetteville, N.Y.) · 2017Article
- Epigenetic Modifications, Alcoholic Brain and Potential Drug Targets.Annals of neurosciences · 2016Review
- The relationship between apoptosis, chromatin configuration, histone modification and competence of oocytes: A study using the mouse ovary-holding stress model.Scientific reports · 2016Article
- The Impact of External Factors on the Epigenome: In Utero and over Lifetime.BioMed research international · 2016Review
- In Vivo Acute on Chronic Ethanol Effects in Liver: A Mouse Model Exhibiting Exacerbated Injury, Altered Metabolic and Epigenetic Responses.Biomolecules · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purposeEthanol binge augments liver injury after chronic ethanol consumption in humans, but the mechanism behind the enhanced liver injury by ethanol binge is not known. In this study we used a clinically relevant rat model in which liver injury is amplified by binge after chronic ethanol treatment and investigated the importance of histone modifications.
methodsEight-week-old Sprague-Dawley rats were fed ethanol in a liquid diet for 4 weeks. Control rats were fed an isocaloric liquid diet. This was followed by three binge administrations of ethanol (intragastric 5 g/kg body weight, 12 h apart). In the control, ethanol was replaced by water. Four hours after the last binge administration, liver samples were analyzed for histone modifications and parameters of liver injury.
resultsChronic ethanol administration alone caused an increase in histone H3 ser10 and ser28 (H3S10 or S28) phosphorylation, and binge ethanol reduced their levels. Levels of dually modified phosphoacetylated histone H3 (H3AcK9/PS10) increased after acute binge ethanol and remained same after chronic ethanol binge. In contrast, histone H3 lysine-9 acetylation (H3AcK9) was not increased after chronic ethanol but increased significantly after acute binge and chronic ethanol binge. Increase in histone acetylation was accompanied by increased phospho-ERK1/2 in the nuclear extracts. Increased acetylation after chronic ethanol binge was also accompanied by increased protein levels of GCN5 histone acetyl transferase and a modest increase in HDAC3 in the nucleus. Histone lysine-9 dimethylation was significantly increased after chronic ethanol binge. Chronic ethanol binge also resulted in a decrease in the SAM:SAH ratio with a relative decrease of SAM levels and a corresponding increase in SAH levels.
conclusionsEthanol binge after chronic ethanol altered the profile of site-specific histone modifications and may underlie the mechanism of augmented liver injury by chronic-ethanol-binge-treated rats.
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