Evidence map›Paper›PMID 25193017›Full record

ArticleNeurotoxicology and teratology

Involvement of seven in absentia homolog-1 in ethanol-induced apoptosis in neural crest cells.

Haijing Sun, Xiaopan Chen, Fuqiang Yuan, Jie Liu, Yingming Zhao, Shao-Yu Chen

Open access · greenAbstract read
In one paragraph

Article in Neurotoxicology and teratology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Fetal Alcohol Exposure: The Common Toll.Journal of alcoholism and drug dependence · 2017
    Article
  8. 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

6 authors at 3 institutions in 1 country.

Haijing SunDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL 61605, United States.
Xiaopan ChenDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL 61605, United States.
Fuqiang YuanDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL 61605, United States.
Jie LiuDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL 61605, United States.
Yingming ZhaoBen May Department for Cancer Research, The University of Chicago, Chicago, IL 60637, United States.
Shao-Yu ChenDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL 61605, United States. Electronic address: sychen@uic.edu.
Illinois College · USUniversity of Chicago · USUniversity of Illinois Urbana-Champaign · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Role of microRNAs in Ethanol-induced Apoptosis and TeratogenesisR01AA021434 · NIAAA · UNIVERSITY OF LOUISVILLE · PI CHEN, SHAO-YU · 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
Role of Nrf2 signaling in modulating ethanol-induced teratogenesisR01AA017446 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CHEN, SHAO-YU · 2008 to 2012
$1.5M
NCATS NIH HHS UL1 TR000430NIAAA NIH HHS AA017446NIAAA NIH HHS AA020265NIAAA NIH HHS AA021434NIAAA NIH HHS R01 AA017446NIAAA NIH HHS R01 AA020265NIAAA NIH HHS R01 AA021434
6 · The paper itself

Abstract

Ethanol-induced apoptosis in selected cell populations is a major component of pathogenesis underlying ethanol-induced teratogenesis. However, there is a fundamental gap in understanding how ethanol leads to apoptosis in embryos. In this study, we investigate the role of seven in absentia homolog-1 (Siah1) protein, an E3 ubiquitin ligase, in ethanol-induced apoptosis. Using an in vitro model of neural crest cell (NCC), JoMa1.3 cells, we found that exposure to 100mM ethanol resulted in a significant increase in Siah1 mRNA expression in NCCs, an ethanol-sensitive cell population implicated in Fetal Alcohol Spectrum Disorders (FASD). Treatment with 100mM ethanol for 24h also significantly increased the protein expression of Siah1 in JoMa1.3 cells. The nuclear translocation and accumulation of Siah1 was evidenced in the cells exposed to ethanol. In addition, we have found that the inhibition of Siah1 function with siRNA prevents ethanol-induced increase in Siah1 protein expression and nuclear translocation in NCCs. Down-regulation of Siah1 by siRNA also greatly diminished ethanol-induced cell death and caspase-3 activation, indicating that inhibition of Siah1 can attenuate ethanol-induced apoptosis. These results strongly suggest that Siah1 plays an important role in ethanol-induced apoptosis in NCCs.

Indexed as

AnimalsApoptosisCaspase 3Cells, CulturedCell SurvivalEthanolMiceNeural CrestNuclear ProteinsRNA, MessengerSeven in Absentia ProteinsUbiquitin-Protein LigasesCaspase 3EthanolNuclear ProteinsRNA, MessengerSeven in Absentia ProteinsUbiquitin-Protein LigasesApoptosisEthanolFetal Alcohol Spectrum DisordersNeural crest cellsSiah1

Identifiers

PMID25193017
PMCPMC4250320
OpenAlexW2090886752

What OpenQuestion holds

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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.