Evidence map›Paper›PMID 34446099›Full record

ArticleClinical epigenetics2021

Betamethasone administration during pregnancy is associated with placental epigenetic changes with implications for inflammation.

Darina Czamara, Linda Dieckmann, Simone Röh, Sarah Kraemer, Rebecca C Rancourt, Sara Sammallahti, Eero Kajantie, Hannele Laivuori, Johan G Eriksson, Katri Räikkönen and 5 more

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Understanding the role of placental pathophysiology in the development of bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2022
    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

15 authors at 6 institutions in 6 countries.

Darina CzamaraDepartment of Translational Research in Psychiatry, Max-Planck-Institute of Psychiatry, 80804, Munich, Germany.ORCID 0000-0001-7381-904X
Linda DieckmannDepartment of Translational Research in Psychiatry, Max-Planck-Institute of Psychiatry, 80804, Munich, Germany.
Simone RöhDepartment of Translational Research in Psychiatry, Max-Planck-Institute of Psychiatry, 80804, Munich, Germany.
Sarah KraemerInstitute of Medical Psychology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health (BIH), Luisenstr. 57, 10117, Berlin, Germany.
Rebecca C RancourtDepartment of Experimental Obstetrics, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health (BIH), Augustenburger Platz 1, 13353, Berlin, Germany.
Sara SammallahtiDepartment of Child and Adolescent Psychiatry, Erasmus MC, Sophia Children's Hospital, Rotterdam, The Netherlands.
Eero KajantieFinnish Institute for Health and Welfare, Helsinki, Finland.
Hannele LaivuoriInstitute for Molecular Medicine Finland, HiLIFE, University of Helsinki, Helsinki, Finland.
Johan G ErikssonDepartment of General Practice and Primary Care, University of Helsinki, Helsinki, Finland.
Katri RäikkönenDepartment of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Wolfgang HenrichDepartment of Obstetrics, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health (BIH), Augustenburger Platz 1, 13353, Berlin, Germany.
Andreas PlagemannDepartment of Experimental Obstetrics, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health (BIH), Augustenburger Platz 1, 13353, Berlin, Germany.
Elisabeth B Binder *Department of Translational Research in Psychiatry, Max-Planck-Institute of Psychiatry, 80804, Munich, Germany.
Thorsten Braun *Department of Experimental Obstetrics, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health (BIH), Augustenburger Platz 1, 13353, Berlin, Germany.
Sonja Entringer *Institute of Medical Psychology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, and Berlin Institute of Health (BIH), Luisenstr. 57, 10117, Berlin, Germany. sonja.entringer@charite.de.
Humboldt-Universität zu Berlin · DEMax Planck Institute of Psychiatry · DEUniversity of Helsinki · FIAgency for Science, Technology and Research · SGEmory University · USErasmus MC - Sophia Children’s Hospital · NL

Funding

deutsche forschungsgemeinschaft BR2925/3-1,-2,-3deutsche forschungsgemeinschaft PL241/8-2,-3
6 · The paper itself

Abstract

backgroundGlucocorticoids (GCs) play a pivotal role in fetal programming. Antenatal treatment with synthetic GCs (sGCs) in individuals in danger of preterm labor is common practice. Adverse short- and long-term effects of antenatal sGCs have been reported, but their effects on placental epigenetic characteristics have never been systematically studied in humans.

resultsWe tested the association between exposure to the sGC betamethasone (BET) and placental DNA methylation (DNAm) in 52 exposed cases and 84 gestational-age-matched controls. We fine-mapped associated loci using targeted bisulfite sequencing. The association of placental DNAm with gene expression and co-expression analysis on implicated genes was performed in an independent cohort including 494 placentas. Exposure to BET was significantly associated with lower placenta DNAm at an enhancer of FKBP5. FKBP5 (FK506-binding protein 51) is a co-chaperone that modulates glucocorticoid receptor activity. Lower DNAm at this enhancer site was associated with higher expression of FKBP5 and a co-expressed gene module. This module is enriched for genes associated with preeclampsia and involved in inflammation and immune response.

conclusionsOur findings suggest that BET exposure during pregnancy associates with few but lasting changes in placental DNAm and may promote a gene expression profile associated with placental dysfunction and increased inflammation. This may represent a pathway mediating GC-associated negative long-term consequences and health outcomes in offspring.

Indexed as

AdultBetamethasoneCohort StudiesDNA MethylationEpigenesis, GeneticFemaleGlucocorticoidsHumansInflammationObstetric Labor ComplicationsPlacentaPregnancyYoung AdultBetamethasoneGlucocorticoidsBetamethasoneDNA methylationFKBP5Gene expressionPlacentaTargeted bisulfite sequencing

Identifiers

PMID34446099
PMCPMC8393766
OpenAlexW3194500484

What OpenQuestion holds

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LicenceCC BY
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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.