Evidence map›Paper›PMID 22324771›Full record

ArticleAlcoholism, clinical and experimental research2012

Metabolic biomarkers of prenatal alcohol exposure in human embryonic stem cell-derived neural lineages.

Jessica A Palmer, Ashley M Poenitzsch, Susan M Smith, Kevin R Conard, Paul R West, Gabriela G Cezar

Open access · bronzeAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.5field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

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  10. The kynurenine pathway in stem cell biology.International journal of tryptophan research : IJTR · 2013
    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

6 authors at 2 institutions in 1 country.

Jessica A PalmerDepartment of Animal Sciences, University of Wisconsin-Madison, USA.
Ashley M Poenitzsch
Susan M Smith
Kevin R Conard
Paul R West
Gabriela G Cezar
University of Wisconsin–Madison · USStemina Biomarker Discovery (United States) · US

Funding

WISCONSIN CENTER ON MENTAL RETARDATION: CORE SUPPORTP30HD003352 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI MESSING, ALBEE · 1985 to 2015
$25.2M
Craniofacial Morphogenesis in Prenatal Alcohol ExposureR01AA011085 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SMITH, SUSAN M. · 2001 to 2025
$6.3M
Craniofacial Morphogenesis in Prenatal Alcohol ExposureR37AA011085 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SMITH, SUSAN M. · 2007 to 2016
$3.3M
Is Maternal Iron Status a Risk Factor in Fetal Alcohol Syndrome?R21AA017281 · NIAAA · UNIVERSITY OF WISCONSIN-MADISON · PI SMITH, SUSAN M. · 2009 to 2010
$399k
Biochemical pathways and biomarkers of alcohol injury in early human developmentR21AA016958 · NIAAA · UNIVERSITY OF WISCONSIN-MADISON · PI CEZAR, GABRIELA G · 2008 to 2009
$353k
CRANIOFACIAL MORPHOGENESIS IN PRENATAL ALCOHOL EXPOSURER29AA011085 · NIAAA · UNIVERSITY OF WISCONSIN MADISON · PI SMITH, SUSAN M. · 1996 to 2000
$100k
NIAAA NIH HHS AA11085NIAAA NIH HHS AA16958NIAAA NIH HHS R01 AA011085NIAAA NIH HHS R21 AA016958NIAAA NIH HHS R21 AA017281NIAAA NIH HHS R29 AA011085NIAAA NIH HHS R37 AA011085NICHD NIH HHS P30 HD003352
6 · The paper itself

Abstract

backgroundFetal alcohol spectrum disorders (FASD) are a leading cause of neurodevelopmental disability. The mechanisms underlying FASD are incompletely understood, and biomarkers to identify those at risk are lacking. Here, we perform metabolomic analysis of embryoid bodies and neural lineages derived from human embryonic stem (hES) cells to identify the neural secretome produced in response to ethanol (EtOH) exposure.

methodsWA01 and WA09 hES cells were differentiated into embryoid bodies, neural progenitors, or neurons. Cells along this progression were cultured for 4 days with 0, 0.1, or 0.3% EtOH. Supernatants were subjected to C18 chromatography followed by ESI-QTOF-MS. Features were annotated using public databases, and the identities of 4 putative biomarkers were confirmed with purified standards and comparative MS/MS.

resultsEtOH treatment induced statistically significant changes to metabolite abundance in human embryoid bodies (180 features), neural progenitors (76 features), and neurons (42 features). There were no shared significant features between different cell types. Fifteen features showed a dose-response to EtOH. Four chemical identities were confirmed: L-thyroxine, 5'-methylthioadenosine, and the tryptophan metabolites, L-kynurenine and indoleacetaldehyde. One feature with a putative annotation of succinyladenosine was significantly increased in both EtOH treatments. Additional features were selective to EtOH treatment but were not annotated in public databases.

conclusionsEtOH exposure induces statistically significant changes to the metabolome profile of human embryoid bodies, neural progenitors, and neurons. Several of these metabolites are normally present in human serum, suggesting their usefulness as potential serum FASD biomarkers. These findings suggest the biochemical pathways that are affected by EtOH in the developing nervous system and delineate mechanisms of alcohol injury during human development.

Indexed as

AdultApoptosisBiomarkersCell CountCell LineageCells, CulturedCentral Nervous System DepressantsDatabases, GeneticDose-Response Relationship, DrugEmbryonic DevelopmentEmbryonic Stem CellsEthanolFemaleHumansImmunohistochemistryMetabolomicsBiomarkersCentral Nervous System DepressantsEthanol

Identifiers

PMID22324771
PMCPMC3374055
OpenAlexW2140736931

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.