Evidence map›Paper›PMID 23340501›Full record

ArticleTranslational psychiatry2013

Differential gene body methylation and reduced expression of cell adhesion and neurotransmitter receptor genes in adverse maternal environment.

J-E Oh, N Chambwe, S Klein, J Gal, S Andrews, G Gleason, R Shaknovich, A Melnick, F Campagne, M Toth

Abstract read
In one paragraph

Article in Translational psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Epigenetic Neuropharmacology: Drugs Affecting the Epigenome in the Brain.Annual review of pharmacology and toxicology · 2021
    Review
  6. Review
  7. The adaptive brain in mental health: overcoming inherited risk factors.Journal of psychiatry & neuroscience : JPN · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Epigenetic Modifications of Major Depressive Disorder.International journal of molecular sciences · 2016
    Review
  12. Review
  13. Article
  14. Principles Governing DNA Methylation during Neuronal Lineage and Subtype Specification.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

10 authors.

J-E OhDepartment of Pharmacology, Weill Cornell Medical College, New York, NY, USA. jio2002@med.cornell.edu
N Chambwe
S Klein
J Gal
S Andrews
G Gleason
R Shaknovich
A Melnick
F Campagne
M Toth

Funding

NEUROBIOLOGY OF ANXIETY IN MICE LACKING 5HT 1A RECEPTORR01MH058669 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI TOTH, MIKLOS · 2000 to 2010
$3.1M
Neuronal CpG Methylation During Development in Normal and Adverse EnvironmentR01MH094720 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI TOTH, MIKLOS · 2011 to 2015
$2.1M
Non-Genetic Transmission of Genetic Risk: Mechanism and Relevance to PsychiatricR01MH086883 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI TOTH, MIKLOS · 2009 to 2012
$1.3M
NIMH NIH HHS 1R01MH58669NIMH NIH HHS 5R01MH086883NIMH NIH HHS R01 MH058669NIMH NIH HHS R01 MH086883NIMH NIH HHS R01 MH094720
6 · The paper itself

Abstract

Early life adversity, including adverse gestational and postpartum maternal environment, is a contributing factor in the development of autism, attention deficit hyperactivity disorder (ADHD), anxiety and depression but little is known about the underlying molecular mechanism. In a model of gestational maternal adversity that leads to innate anxiety, increased stress reactivity and impaired vocal communication in the offspring, we asked if a specific DNA methylation signature is associated with the emergence of the behavioral phenotype. Genome-wide DNA methylation analyses identified 2.3% of CpGs as differentially methylated (that is, differentially methylated sites, DMSs) by the adverse environment in ventral-hippocampal granule cells, neurons that can be linked to the anxiety phenotype. DMSs were typically clustered and these clusters were preferentially located at gene bodies. Although CpGs are typically either highly methylated or unmethylated, DMSs had an intermediate (20-80%) methylation level that may contribute to their sensitivity to environmental adversity. The adverse maternal environment resulted in either hyper or hypomethylation at DMSs. Clusters of DMSs were enriched in genes that encode cell adhesion molecules and neurotransmitter receptors; some of which were also downregulated, indicating multiple functional deficits at the synapse in adversity. Pharmacological and genetic evidence links many of these genes to anxiety.

Indexed as

AnimalsAnxietyCell AdhesionCpG IslandsDentate GyrusDisease Models, AnimalDNA MethylationEpigenesis, GeneticFemaleMaleMiceMice, TransgenicPregnancyPrenatal Exposure Delayed EffectsReceptor, Serotonin, 5-HT1AVocalization, AnimalReceptor, Serotonin, 5-HT1A

Identifiers

PMID23340501
PMCPMC3566713

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Registered trials

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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.