Evidence map›Paper›PMID 32066736›Full record

ArticleTranslational psychiatry2020

Stress genomics revisited: gene co-expression analysis identifies molecular signatures associated with childhood adversity.

Linda Dieckmann, Steve Cole, Robert Kumsta

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Article
  5. Review
  6. Transcriptomics and psychotherapy: An integrative review.Brain, behavior, & immunity - health · 2024
    Review
  7. Observational
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  14. Ecoimmunology in the field: Measuring multiple dimensions of immune function with minimally invasive, field-adapted techniques.American journal of human biology : the official journal of the Human Biology Council · 2022
    Review
  15. Article
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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

3 authors at 3 institutions in 2 countries.

Linda DieckmannDepartment of Genetic Psychology, Faculty of Psychology, Ruhr University Bochum, Bochum, Germany.
Steve ColeDivision of Hematology/Oncology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Robert KumstaDepartment of Genetic Psychology, Faculty of Psychology, Ruhr University Bochum, Bochum, Germany. robert.kumsta@rub.de.ORCID http://orcid.org/0000-0001-6006-6958
Ruhr University Bochum · DEUniversity Hospitals of the Ruhr-University of Bochum · DEUniversity of California, Los Angeles · US

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) KU 2479/3-1; KU 2479/3-2
6 · The paper itself

Abstract

Childhood adversity is related to an increased risk for psychopathology in adulthood. Altered regulation of stress response systems, as well as the changes in stress-immune interplay have been suggested as potential mechanisms underlying these long-term effects. We have previously shown altered transcriptional responses to acute psychosocial stress in adults reporting the experience of childhood adversity. Here, we extend these analyses using a network approach. We performed a co-expression network analysis of genome-wide mRNA data derived from isolated monocytes, sampled 3 h after stress exposure from healthy adults, who experienced childhood adversity and a matched control group without adverse childhood experiences. Thirteen co-expression modules were identified, of which four modules were enriched for genes related to immune system function. Gene set enrichment analysis showed differential module activity between the early adversity and control group. In line with previous findings reporting a pro-inflammatory bias following childhood adversity, one module included genes associated with pro-inflammatory function (hub genes: IL6, TM4SF1, ADAMTS4, CYR61, CCDC3), more strongly expressed in the early adversity group. Another module downregulated in the early adversity group was related to platelet activation and wound healing (hub genes: GP9, CMTM5, TUBB1, GNG11, PF4), and resembled a co-expression module previously found over-expressed in post-traumatic stress disorder resilient soldiers. These discovery analysis results provide a system wide and more holistic understanding of gene expression programs associated with childhood adversity. Furthermore, identified hub genes can be used in directed hypothesis testing in future studies.

Indexed as

Adverse Childhood ExperiencesStress Disorders, Post-TraumaticAdultChemokinesGene ExpressionGenomicsHumansMARVEL Domain-Containing ProteinsPsychopathologyTumor Suppressor ProteinsChemokinesCMTM5 protein, humanMARVEL Domain-Containing ProteinsTumor Suppressor Proteins

Identifiers

PMID32066736
PMCPMC7026041
OpenAlexW3002407307

What OpenQuestion holds

Textmetadata
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.