Evidence map›Paper›PMID 31247197›Full record

ArticleExperimental neurology2019

MicroRNA-34a mediates ethanol-induced impairment of neural differentiation of neural crest cells by targeting autophagy-related gene 9a.

Huadong Fan, Fuqiang Yuan, Yang Yun, Ting Wu, Lanhai Lu, Jie Liu, Wenke Feng, Shao-Yu Chen

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  3. Acute exposure to electronic cigarette components alters mRNA expression of pre-osteoblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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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

8 authors at 1 institution in 2 countries.

Huadong FanDepartment of Pharmacology and Toxicology, University of Louisville Health Science Center, Louisville, KY 40202, USA; University of Louisville Alcohol Research Center, Louisville, KY 40202, USA. Electronic address: Huadong.Fan@louisville.edu.
Fuqiang YuanDepartment of Pharmacology and Toxicology, University of Louisville Health Science Center, Louisville, KY 40202, USA; University of Louisville Alcohol Research Center, Louisville, KY 40202, USA. Electronic address: Fuqiang.Yuan@louisville.edu.
Yang YunDepartment of Pharmacology and Toxicology, University of Louisville Health Science Center, Louisville, KY 40202, USA; University of Louisville Alcohol Research Center, Louisville, KY 40202, USA; College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi, China.
Ting WuDepartment of Pharmacology and Toxicology, University of Louisville Health Science Center, Louisville, KY 40202, USA; University of Louisville Alcohol Research Center, Louisville, KY 40202, USA. Electronic address: ting.wu@louisville.edu.
Lanhai LuDepartment of Pharmacology and Toxicology, University of Louisville Health Science Center, Louisville, KY 40202, USA; University of Louisville Alcohol Research Center, Louisville, KY 40202, USA. Electronic address: lanhai.lu@louisville.edu.
Jie LiuDepartment of Pharmacology and Toxicology, University of Louisville Health Science Center, Louisville, KY 40202, USA; University of Louisville Alcohol Research Center, Louisville, KY 40202, USA. Electronic address: jie.liu@louisville.edu.
Wenke FengUniversity of Louisville Alcohol Research Center, Louisville, KY 40202, USA; Department of Medicine, University of Louisville, Louisville, KY 40292, USA. Electronic address: wenke.feng@louisville.edu.
Shao-Yu ChenDepartment of Pharmacology and Toxicology, University of Louisville Health Science Center, Louisville, KY 40202, USA; University of Louisville Alcohol Research Center, Louisville, KY 40202, USA. Electronic address: shaoyu.chen@louisville.edu.
University of Louisville · US

Funding

The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI CRAIG J. MCCLAIN · 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
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 AA022416
6 · The paper itself

Abstract

Neural crest cells (NCCs) are multipotent progenitor cells that are sensitive to ethanol and are implicated in Fetal Alcohol Spectrum Disorders (FASD). The objective of this study is to test whether ethanol exposure can inhibit the neural differentiation of NCCs by inhibiting autophagy and whether miR-34a is involved in ethanol-induced inhibition of autophagy in NCCs. We found that ethanol exposure resulted in the inhibition of neural differentiation of NCCs. Exposure to ethanol also significantly decreased autophagy in NCCs, as indicated by a decreased LC3II/I ratio and an elevated expression of p62 protein. Knockdown of p62 restored the expression of the neurogenesis genes, NF and Mash1, in ethanol-exposed NCCs, suggesting that ethanol exposure can inhibit the neural differentiation of NCCs by inhibiting autophagy. We also found that ethanol exposure resulted in a significant increase in miR-34a expression in NCCs. Inhibition of miR-34a restored the expression of Atg9a, a direct target of miR-34a and significantly decreased ethanol-induced inhibition of autophagy in NCCs. Down-regulation of miR-34a also prevented ethanol-induced inhibition of neural differentiation of NCCs. These results demonstrate that ethanol-induced inhibition of neural differentiation of NCCs is mediated by the miR-34a through targeting Atg9a.

Indexed as

AnimalsAutophagyAutophagy-Related ProteinsCell DifferentiationCell LineEthanolMembrane ProteinsMiceMicroRNAsNeural CrestVesicular Transport ProteinsAtg9A protein, mouseAutophagy-Related ProteinsEthanolMembrane ProteinsMicroRNAsMIRN34a microRNA, mouseVesicular Transport ProteinsAtg9aAutophagyDifferentiationEthanolmiR-34aNeural crest cell

Identifiers

PMID31247197
PMCPMC6708457
OpenAlexW2953912707

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.