Evidence map›Paper›PMID 26266540›Full record

ArticlePloS one2015

Ethanol upregulates NMDA receptor subunit gene expression in human embryonic stem cell-derived cortical neurons.

Yangfei Xiang, Kun-Yong Kim, Joel Gelernter, In-Hyun Park, Huiping Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 63 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Yangfei XiangDepartment of Genetics, Yale University School of Medicine, New Haven, CT, United States of America.
Kun-Yong KimDepartment of Genetics, Yale University School of Medicine, New Haven, CT, United States of America.
Joel GelernterDepartment of Genetics, Yale University School of Medicine, New Haven, CT, United States of America; Department of Psychiatry, Yale University School of Medicine, New Haven, CT, United States of America; Department of Neurobiology, Yale University School of Medicine, New Haven, CT, United States of America; VA Medical Center, VA Connecticut Healthcare System, West Haven, CT, United States of America.
In-Hyun ParkDepartment of Genetics, Yale University School of Medicine, New Haven, CT, United States of America.
Huiping ZhangDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT, United States of America; VA Medical Center, VA Connecticut Healthcare System, West Haven, CT, United States of America.
Yale University · USVA Connecticut Healthcare System · US

Funding

Translational Technologies CoreP50AA012870 · NIAAA · YALE UNIVERSITY · PI Matthew J Girgenti · 2001 to 2026
$43.7M
Investigation of the function of methylated DNA binding protein in reprogrammingR01GM111667 · NIGMS · YALE UNIVERSITY · PI PARK, IN-HYUN · 2014 to 2018
$1.6M
Salivary MicroRNAs as Biomarkers for Alcohol DependenceR21AA023068 · NIAAA · YALE UNIVERSITY · PI ZHANG, HUIPING · 2015 to 2016
$344k
NIAAA NIH HHS P50 AA012870NIAAA NIH HHS P50 AA12870NIAAA NIH HHS R21 AA023068NIGMS NIH HHS R01 GM111667
6 · The paper itself

Abstract

Chronic alcohol consumption may result in sustained gene expression alterations in the brain, leading to alcohol abuse or dependence. Because of ethical concerns of using live human brain cells in research, this hypothesis cannot be tested directly in live human brains. In the present study, we used human embryonic stem cell (hESC)-derived cortical neurons as in vitro cellular models to investigate alcohol-induced expression changes of genes involved in alcohol metabolism (ALDH2), anti-apoptosis (BCL2 and CCND2), neurotransmission (NMDA receptor subunit genes: GRIN1, GRIN2A, GRIN2B, and GRIN2D), calcium channel activity (ITPR2), or transcriptional repression (JARID2). hESCs were differentiated into cortical neurons, which were characterized by immunostaining using antibodies against cortical neuron-specific biomarkers. Ethanol-induced gene expression changes were determined by reverse-transcription quantitative polymerase chain reaction (RT-qPCR). After a 7-day ethanol (50 mM) exposure followed by a 24-hour ethanol withdrawal treatment, five of the above nine genes (including all four NMDA receptor subunit genes) were highly upregulated (GRIN1: 1.93-fold, P = 0.003; GRIN2A: 1.40-fold, P = 0.003; GRIN2B: 1.75-fold, P = 0.002; GRIN2D: 1.86-fold, P = 0.048; BCL2: 1.34-fold, P = 0.031), and the results of GRIN1, GRIN2A, and GRIN2B survived multiple comparison correction. Our findings suggest that alcohol responsive genes, particularly NMDA receptor genes, play an important role in regulating neuronal function and mediating chronic alcohol consumption-induced neuroadaptations.

Indexed as

Alcohol DrinkingCell DifferentiationCerebral CortexEthanolGene Expression RegulationHuman Embryonic Stem CellsHumansNeuronsSignal TransductionSynaptic TransmissionTranscriptional ActivationEthanol

Identifiers

PMID26266540
PMCPMC4534442
OpenAlexW1447824855

What OpenQuestion holds

Textmetadata
LicenceCC0
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.