Evidence map›Paper›PMID 29069573›Full record

ArticleExperimental neurology2018

Sulforaphane restores acetyl-histone H3 binding to Bcl-2 promoter and prevents apoptosis in ethanol-exposed neural crest cells and mouse embryos.

Fuqiang Yuan, Xiaopan Chen, Jie Liu, Wenke Feng, Lu Cai, Xiaoyang Wu, Shao-Yu Chen

Abstract read
In one paragraph

Article in Experimental neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  8. Immunomodulatory Effects of (Pharmaceuticals (Basel, Switzerland) · 2022
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  10. Review
  11. Impact of Alcohol Consumption on Male Fertility Potential: A Narrative Review.International journal of environmental research and public health · 2021
    Review
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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

7 authors at 3 institutions in 2 countries.

Fuqiang YuanDepartment of Pharmacology and Toxicology, University of Louisville Health Sciences Center, Louisville, KY 40202, USA; University of Louisville, Alcohol Research Center, Louisville, KY 40202, USA.
Xiaopan ChenDepartment of Pharmacology and Toxicology, University of Louisville Health Sciences Center, Louisville, KY 40202, USA; University of Louisville, Alcohol Research Center, Louisville, KY 40202, USA; Department of Reproductive Endocrinology, Zhejiang Provincial People's Hospital, 158 Shangtang Road, Hangzhou, Zhejiang 310014, China.
Jie LiuDepartment of Pharmacology and Toxicology, University of Louisville Health Sciences Center, Louisville, KY 40202, USA; University of Louisville, Alcohol Research Center, Louisville, KY 40202, USA.
Wenke FengUniversity of Louisville, Alcohol Research Center, Louisville, KY 40202, USA; Department of Medicine, University of Louisville, Louisville, KY 40292, USA.
Lu CaiPediatric Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA.
Xiaoyang WuBen May Department for Cancer Research, University of Chicago, Chicago, IL 60637, USA.
Shao-Yu ChenDepartment of Pharmacology and Toxicology, University of Louisville Health Sciences Center, Louisville, KY 40202, USA; University of Louisville, Alcohol Research Center, Louisville, KY 40202, USA. Electronic address: shaoyu.chen@louisville.edu.
University of Louisville · USUniversity of Chicago · USZhejiang Provincial People's Hospital · CN

Funding

Role of oxidized linoleic acid metabolites in the pathogenesis of alcoholic liver diseaseP20GM113226 · NIGMS · UNIVERSITY OF LOUISVILLE · PI GHARE, SMITA S · 2016 to 2025
$24.1M
The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI SHIRISH S BARVE · 2016 to 2026
$17.9M
Mechanisms of Probiotics in Alcoholic Liver DiseaseR01AA023190 · NIAAA · UNIVERSITY OF LOUISVILLE · PI FENG, WENKE · 2015 to 2024
$3.5M
Role of microRNAs in Ethanol-induced Apoptosis and TeratogenesisR01AA021434 · NIAAA · UNIVERSITY OF LOUISVILLE · PI CHEN, SHAO-YU · 2013 to 2017
$1.7M
Coordinated cytoskeletal dynamics in skin somatic stem cells - Resubmission 01R01AR063630 · NIAMS · UNIVERSITY OF CHICAGO · PI WU, XIAOYANG · 2013 to 2017
$1.7M
Role of Siah1 in ethanol-induced apoptosis and teratogenesisR01AA020265 · NIAAA · UNIVERSITY OF LOUISVILLE · PI CHEN, SHAO-YU · 2012 to 2016
$1.7M
FGF21 and adipose lipolysis in alcoholic fatty liverR21AA022416 · NIAAA · UNIVERSITY OF LOUISVILLE · PI FENG, WENKE · 2014 to 2015
$388k
NIAAA NIH HHS P50 AA024337NIAAA NIH HHS R01 AA020265NIAAA NIH HHS R01 AA021434NIAAA NIH HHS R01 AA023190NIAAA NIH HHS R21 AA022416NIAMS NIH HHS R01 AR063630NIGMS NIH HHS P20 GM113226
6 · The paper itself

Abstract

Sulforaphane (SFN) is an isothiocyanate derived from cruciferous vegetables. SFN's cytoprotective properties have been demonstrated in several models associated with a variety of disorders. Our recent studies have shown that SFN protects against ethanol-induced oxidative stress and apoptosis in neural crest cells (NCCs), an ethanol-sensitive cell population implicated in Fetal Alcohol Spectrum Disorders (FASD). This study is designed to test the hypothesis that SFN can prevent ethanol-induced apoptosis in NCCs by inhibiting HDAC and increasing histone acetylation at the Bcl-2 promoter. We found that exposure to 50mM ethanol resulted in a significant increase in HDAC activities in NCCs. Treatment with SFN decreased the activities of HDAC in ethanol-exposed NCCs. We also found that SFN treatment significantly increased the expression of acetyl-histone H3 in NCCs treated with ethanol. ChIP-qPCR assay revealed that ethanol exposure significantly decreased acetyl-histone H3 binding to the Bcl-2 promoter while supplementing with SFN reversed the ethanol-induced reduction in acetyl-histone H3 binding to the Bcl-2 promoter. In addition, SFN treatment restored the expression of Bcl-2 in ethanol-exposed NCCs and diminished ethanol-induced apoptosis in NCCs. Treatment with SFN also significantly diminished apoptosis in mouse embryos exposed to ethanol in vivo. These results demonstrate that SFN can epigenetically restore the expression of Bcl-2 and attenuate ethanol-induced apoptosis by increasing histone acetylation at the Bcl-2 promoter and suggest that SFN may prevent FASD through epigenetic regulation of the expression of anti-apoptotic genes.

Indexed as

AnimalsApoptosisCells, CulturedEmbryonic DevelopmentEnzyme ActivationEthanolFemaleHistonesIsothiocyanatesMiceMice, Inbred C57BLNeural CrestPregnancyPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-bcl-2EthanolHistonesIsothiocyanatesProto-Oncogene Proteins c-bcl-2sulforaphaneSulfoxidesApoptosisBcl-2EthanolHistone deacetylaseSulforaphane

Identifiers

PMID29069573
PMCPMC5745274
OpenAlexW2766295686

What OpenQuestion holds

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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.