Evidence map›Paper›PMID 22301686›Full record

ArticleAlcohol and alcoholism (Oxford, Oxfordshire)

Gene-selective histone H3 acetylation in the absence of increase in global histone acetylation in liver of rats chronically fed alcohol.

Pil-Hoon Park, Robert W Lim, Shivendra D Shukla

Open access · bronzeAbstract read
In one paragraph

Article in Alcohol and alcoholism (Oxford, Oxfordshire). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Epigenetics of alcohol-related liver diseases.JHEP reports : innovation in hepatology · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Homocysteine, Alcoholism, and Its Potential Epigenetic Mechanism.Alcoholism, clinical and experimental research · 2016
    Review
  16. Article
  17. Article
  18. Sirtuin 1 signaling and alcoholic fatty liver disease.Hepatobiliary surgery and nutrition · 2015
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Pil-Hoon ParkCollege of Pharmacy, Yeungnam University, Gyeongsan, Gyeongsangbuk-do, Republic of Korea.
Robert W Lim
Shivendra D Shukla
University of Missouri · USYeungnam University · KR

Funding

Histone Modifications by Ethanol: Mechanism & ConsequenceR01AA016347 · NIAAA · UNIVERSITY OF MISSOURI-COLUMBIA · PI SHUKLA, SHIVENDRA D · 2007 to 2011
$1.6M
NIAAA NIH HHS AA16347
6 · The paper itself

Abstract

aimsThe aim of this study was to determine the effect of chronic ethanol feeding on acetylation of histone H3 at lysine 9 (H3-Lys9) at promoter and coding regions of genes for class I alcohol dehydrogenase (ADH I), inducible nitric oxide synthase (iNOS), Bax, p21, c-met and hepatocyte growth factor in the rat liver.

methodsRats were fed ethanol-containing liquid diet (5%, w/v) for 1-4 weeks. The global level of acetylation of H3-Lys9 in the liver was examined by western blot analysis. The levels of mRNA for various genes were measured by real-time reverse transcriptase-polymerase chain reaction. The association of acetylated histone H3-Lys9 with the different regions of genes was monitored by chromatin immunoprecipitation assay.

resultsChronic ethanol treatment increased mRNA expression of genes for iNOS, c-jun and ADH 1. Chronic ethanol treatment did not cause increase in global acetylation of H3-Lys9, but significantly increased the association of acetylated histone H3-Lys9 in the ADH I gene, both in promoter and in coding regions. In contrast, chronic ethanol treatment did not significantly increase the association of acetylated histone H3-Lys9 with iNOS and c-jun genes.

conclusionChronic ethanol exposure increased the gene-selective association of acetylated H3-Lys9 in the absence of global histone acetylation. Thus, not all genes expressed by ethanol are linked to transcription via histone H3 acetylation at Lys9.

Indexed as

AcetylationAlcohol DehydrogenaseAnimalsbcl-2-Associated X ProteinCentral Nervous System DepressantsEthanolGene ExpressionGenes, junHepatocyte Growth FactorHistonesLiverLysineMaleNitric Oxide Synthase Type IIPromoter Regions, GeneticProtein Processing, Post-TranslationalAlcohol Dehydrogenasebcl-2-Associated X ProteinCentral Nervous System DepressantsEthanolHepatocyte Growth FactorHistonesLysineNitric Oxide Synthase Type IIProto-Oncogene Proteins c-metRNA, Messenger

Identifiers

PMID22301686
PMCPMC3331618
OpenAlexW2120554401

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.