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dc.contributor.authorCzamara, Darina
dc.contributor.authorDieckmann, Linda
dc.contributor.authorRöh, Simone
dc.contributor.authorKraemer, Sarah
dc.contributor.authorRancourt, Rebecca C.
dc.contributor.authorSammallahti, Sara
dc.contributor.authorKajantie, Eero Olavi
dc.contributor.authorLaivuori, Hannele
dc.contributor.authorEriksson, Johan G.
dc.contributor.authorRäikkönen, Katri
dc.contributor.authorHenrich, Wolfgang
dc.contributor.authorPlagemann, Andreas
dc.contributor.authorBinder, Elisabeth B.
dc.contributor.authorBraun, Thorsten
dc.contributor.authorEntringer, Sonja
dc.date.accessioned2023-01-23T09:15:18Z
dc.date.available2023-01-23T09:15:18Z
dc.date.created2022-01-11T11:19:36Z
dc.date.issued2021
dc.identifier.citationClinical Epigenetics. 2021, 13 (1), .en_US
dc.identifier.issn1868-7075
dc.identifier.urihttps://hdl.handle.net/11250/3045171
dc.description.abstractBackground Glucocorticoids (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. Results We 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. Conclusions Our 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.en_US
dc.language.isoengen_US
dc.publisherBioMed Centralen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleBetamethasone administration during pregnancy is associated with placental epigenetic changes with implications for inflammationen_US
dc.title.alternativeBetamethasone administration during pregnancy is associated with placental epigenetic changes with implications for inflammationen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.source.pagenumber17en_US
dc.source.volume13en_US
dc.source.journalClinical Epigeneticsen_US
dc.source.issue1en_US
dc.identifier.doi10.1186/s13148-021-01153-y
dc.identifier.cristin1978126
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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