Evidence map›Paper›PMID 25970770›Full record

ArticlePloS one2015

Early maternal alcohol consumption alters hippocampal DNA methylation, gene expression and volume in a mouse model.

Heidi Marjonen, Alejandra Sierra, Anna Nyman, Vladimir Rogojin, Olli Gröhn, Anni-Maija Linden, Sampsa Hautaniemi, Nina Kaminen-Ahola

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 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
16.7field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

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  12. Mitigating the detrimental developmental impact of early fetal alcohol exposure using a maternal methyl donor-enriched diet.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
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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 2 institutions in 1 country.

Heidi MarjonenDepartment of Medical Genetics, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Alejandra SierraDepartment of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
Anna NymanDepartment of Medical Genetics, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Vladimir RogojinInstitute of Biomedicine & Genome-Scale Biology Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Olli GröhnDepartment of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
Anni-Maija LindenInstitute of Biomedicine, Pharmacology, University of Helsinki, Helsinki, Finland.
Sampsa HautaniemiInstitute of Biomedicine & Genome-Scale Biology Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Nina Kaminen-AholaDepartment of Medical Genetics, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
University of Helsinki · FIUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adverse effects of alcohol consumption during pregnancy are known, but the molecular events that lead to the phenotypic characteristics are unclear. To unravel the molecular mechanisms, we have used a mouse model of gestational ethanol exposure, which is based on maternal ad libitum ingestion of 10% (v/v) ethanol for the first 8 days of gestation (GD 0.5-8.5). Early neurulation takes place by the end of this period, which is equivalent to the developmental stage early in the fourth week post-fertilization in human. During this exposure period, dynamic epigenetic reprogramming takes place and the embryo is vulnerable to the effects of environmental factors. Thus, we hypothesize that early ethanol exposure disrupts the epigenetic reprogramming of the embryo, which leads to alterations in gene regulation and life-long changes in brain structure and function. Genome-wide analysis of gene expression in the mouse hippocampus revealed altered expression of 23 genes and three miRNAs in ethanol-exposed, adolescent offspring at postnatal day (P) 28. We confirmed this result by using two other tissues, where three candidate genes are known to express actively. Interestingly, we found a similar trend of upregulated gene expression in bone marrow and main olfactory epithelium. In addition, we observed altered DNA methylation in the CpG islands upstream of the candidate genes in the hippocampus. Our MRI study revealed asymmetry of brain structures in ethanol-exposed adult offspring (P60): we detected ethanol-induced enlargement of the left hippocampus and decreased volume of the left olfactory bulb. Our study indicates that ethanol exposure in early gestation can cause changes in DNA methylation, gene expression, and brain structure of offspring. Furthermore, the results support our hypothesis of early epigenetic origin of alcohol-induced disorders: changes in gene regulation may have already taken place in embryonic stem cells and therefore can be seen in different tissue types later in life.

Indexed as

Epigenesis, GeneticAlcohol DrinkingAnimalsBone MarrowCpG IslandsDisease Models, AnimalDNA MethylationEthanolFemaleGene Expression ProfilingGene Expression Regulation, DevelopmentalGenomeHippocampusHistonesHumansImmunoglobulin Light Chains, SurrogateEthanolHistonesImmunoglobulin Light Chains, SurrogateMicroRNAspre-B lymphocyte gene 2 protein, mouseReceptors, Odorant

Identifiers

PMID25970770
PMCPMC4430308
OpenAlexW1866504702

What OpenQuestion holds

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LicenceCC BY
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.