ArticleExperimental and molecular pathology2008
Epigenetic mechanisms regulate Mallory Denk body formation in the livers of drug-primed mice.
Article in Experimental and molecular pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Studies on the functional role of UFMylation in cells (Review).Molecular medicine reports · 2025Review
- Role of Protein Quality Control Failure in Alcoholic Hepatitis Pathogenesis.Biomolecules · 2017Review
- Altered regulation of miR-34a and miR-483-3p in alcoholic hepatitis and DDC fed mice.Experimental and molecular pathology · 2015Article
- Mallory-Denk Body (MDB) formation modulates Ufmylation expression epigenetically in alcoholic hepatitis (AH) and non-alcoholic steatohepatitis (NASH).Experimental and molecular pathology · 2014Article
- Methylation and gene expression responses to ethanol feeding and betaine supplementation in the cystathionine beta synthase-deficient mouse.Alcoholism, clinical and experimental research · 2014Article
- Epigenetic events in liver cancer resulting from alcoholic liver disease.Alcohol research : current reviews · 2013Review
- FAT10 knock out mice livers fail to develop Mallory-Denk bodies in the DDC mouse model.Experimental and molecular pathology · 2012Article
- The role of innate immunity in the pathogenesis of preneoplasia in drug-induced chronic hepatitis based on a mouse model.Experimental and molecular pathology · 2011Review
- The immunoproteasome in steatohepatitis: its role in Mallory-Denk body formation.Experimental and molecular pathology · 2011Article
- Mallory-Denk body pathogenesis revisited.World journal of hepatology · 2010Article
- The role of cytokines in UbD promoter regulation and Mallory-Denk body-like aggresomes.Experimental and molecular pathology · 2010Article
- SAMe prevents the up regulation of toll-like receptor signaling in Mallory-Denk body forming hepatocytes.Experimental and molecular pathology · 2010Article
- SAMe prevents the induction of the immunoproteasome and preserves the 26S proteasome in the DDC-induced MDB mouse model.Experimental and molecular pathology · 2010Article
- Gene expression modifications in the liver caused by binge drinking and S-adenosylmethionine feeding. The role of epigenetic changes.Genes & nutrition · 2010Article
- Molecular events in hepatic preneoplasia: a review.Experimental and molecular pathology · 2010Review
- The role of stem cells/progenitor cells in liver carcinogenesis in glycine N-methyltransferase deficient mice.Experimental and molecular pathology · 2010Article
- Alcohol, nutrition and liver cancer: role of Toll-like receptor signaling.World journal of gastroenterology · 2010Review
- Epigenetic regulation of hepatic endoplasmic reticulum stress pathways in the ethanol-fed cystathionine beta synthase-deficient mouse.Hepatology (Baltimore, Md.) · 2010Article
- Impaired methylation as a novel mechanism for proteasome suppression in liver cells.Biochemical and biophysical research communications · 2010Article
- The regulation of non-coding RNA expression in the liver of mice fed DDC.Experimental and molecular pathology · 2009Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanism of Mallory Denk body formation is still not fully understood, but growing evidence implicates epigenetic mechanisms in MDB formation. In a previous study the epigenetic memory of MDB formation remained intact for at least 4 months after withdrawal from the DDC diet. In the present study, mice were fed a diet containing DDC or a diet containing DDC and S-adenosylmethionine (SAMe) to investigate the epigenetic memory of MDB formation. DDC feeding caused an increase in histone 3 acetylation, a decrease in histone 3 trimethylation, and an increase in histone ubiquitinylation. The addition of SAMe to the DDC diet prevented the DDC induced decrease of H3K4 and H3K9 trimethylation and the increase in histone ubiquitinylation. Changes in histone modifying enzymes (HATs and HDACs), were also found in the liver nuclear extracts of the DDC/SAMe fed mice. Data mining of microarray analysis confirmed that gene expression changed with DDC refeeding, particularly the SAMe metabolizing enzymes, Mat2a, AMD, AHCY and Mthfr. SAMe supplementation prevented the decrease of AHCY and GNMT, and prevented the increase in Mthfr, which provides a mechanism to explain how DDC inhibits methylation of histones. The results indicate that SAMe prevented the epigenetic cellular memory involved in the MDB formation.
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