ArticleExperimental and molecular pathology2010
SAMe prevents the up regulation of toll-like receptor signaling in Mallory-Denk body forming hepatocytes.
Article in Experimental and molecular pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Single-cell transcriptomic analysis reveals characteristic feature of macrophage reprogramming in liver Mallory-Denk bodies pathogenesis.Journal of translational medicine · 2025Article
- Article
- Role of Methylation in Pro- and Anti-Cancer Immunity.Cancers · 2021Review
- Role of Chronic Alcoholism Causing Cancer in Omnivores and Vegetarians through Epigenetic Modifications.Global medical genetics · 2020Review
- The role of Tec kinase signaling pathways in the development of Mallory Denk Bodies in balloon cells in alcoholic hepatitis.Experimental and molecular pathology · 2017Article
- Over expression of proteins that alter the intracellular signaling pathways in the cytoplasm of the liver cells forming Mallory-Denk bodies.Experimental and molecular pathology · 2017Article
- TLR3/4 signaling is mediated via the NFκB-CXCR4/7 pathway in human alcoholic hepatitis and non-alcoholic steatohepatitis which formed Mallory-Denk bodies.Experimental and molecular pathology · 2014Article
- Balloon liver cells forming Mallory-Denk-bodies are progenitor cells.Experimental and molecular pathology · 2013Article
- SAMe treatment prevents the ethanol-induced epigenetic alterations of genes in the Toll-like receptor pathway.Experimental and molecular pathology · 2013Article
- Antioxidant N-acetylcysteine attenuates hepatocarcinogenesis by inhibiting ROS/ER stress in TLR2 deficient mouse.PloS one · 2013Article
- 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
- Mallory-Denk bodies form when EZH2/H3K27me3 fails to methylate DNA in the nuclei of human and mice liver cells.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
- S-adenosylmethionine prevents the up regulation of Toll-like receptor (TLR) signaling caused by chronic ethanol feeding in rats.Experimental and molecular pathology · 2011Article
- The immunoproteasome in steatohepatitis: its role in Mallory-Denk body formation.Experimental and molecular pathology · 2011Article
- Increased expression of FAT10 in colon benign, premalignant and malignant epithelial neoplasms.Experimental and molecular pathology · 2011Article
- Mallory-Denk body pathogenesis revisited.World journal of hepatology · 2010Article
- SAMe prevents the up regulation of toll-like receptor signaling in Mallory-Denk body forming hepatocytes.Experimental and molecular pathology · 2010Article
- Alcohol, nutrition and liver cancer: role of Toll-like receptor signaling.World journal of gastroenterology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Mallory-Denk body (MDB) formation is a component of alcoholic and non alcoholic hepatitis. In the present study, the role of the toll-like receptor (TLR) signaling pathway was investigated in the mechanism of MDB formation in the DDC-fed mouse model. Microarray analysis data mining, performed on the livers of drug-primed mice refed DDC, showed that TLR2/4 gene expression was significantly up regulated by DDC refeeding. SAMe supplementation prevented this up regulation and prevented the formation of MDBs. qRT-PCR analysis confirmed these results. TLR2/4 activates the adapter protein MyD88. The levels of MyD88 were increased by DDC refeeding. The increase of MyD88 was also prevented by SAMe supplementation. Results showed that MyD88-independent TLR3/4-TRIF-IRF3 pathway was not up regulated in the liver of DDC refed mice. Tumor necrosis factor receptor-associated factor 6 (TRAF6) is the downstream protein recruited by the MyD88/IRAK protein complex, and is involved in the regulation of innate immune responses. Results showed a significant increase in the levels of TRAF-6. TRAF-6 activation leads to activation of NFkB and the mitogen-activated protein kinase (MAPK) cascade. The TRAF-6 increase was ameliorated by SAMe supplementation. These results suggest that DDC induces MDB formation through the TLR2/4 and MyD88-dependent signaling pathway. In conclusion, SAMe blocked the over-expression of TLR2/4, and their downstream signaling components MyD88 and TRAF-6. SAMe prevented the DDC-induced up regulation of the TLR signaling pathways, probably by preventing the up regulation of INF-gamma receptors by DDC feeding. INFgamma stimulates the up regulation of TLR2. The ability of SAMe feeding to prevent TLR signaling up regulation has not been previously described.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.