ArticlePloS one2025
Prenatal stress increases corticosterone levels in offspring by impairing placental glucocorticoid barrier function.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Prenatal road traffic noise impairs early testicular development in Sprague-Dawley offspring: pharmacological rescue by melatonin and edaravone; developmental preservation by environmental enrichment.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Comparative Analysis of Prenatal Stress Models: Placental and Neurodevelopmental Outcomes in Mice.The Yale journal of biology and medicine · 2026Article
- Changed expression of placental transporters and disrupted epigenetic patterns in a rat model of schizophrenia.Frontiers in pharmacology · 2025Article
- Prenatal stress and neuroendocrine pathways framing attention-deficit/hyperactivity disorder as a functionally based neurodevelopmental disorder: a narrative review.Journal of Yeungnam medical science · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the association between prenatal stress (PS) and corticosterone levels, and its influence on DNA methylation of genes related to the placental glucocorticoid (GC) barrier, including 11β-HSD2, ABCB1 (P-gp), NR3C1, and FKBP5. The PS model was established through chronic unpredictable mild stress (CUMS). DNA methylation of GC-related genes was analyzed by reduced representation bisulfite sequencing (RRBS), and the results were confirmed using MethylTarget™ sequencing. The mRNA and protein expression levels of these genes were detected through qRT-PCR and Western blotting, respectively. Plasma corticosterone levels were elevated in pregnant female rats exposed to PS conditions and their offspring. Compared to the offspring of the prenatal control (OPC) group, the offspring of the prenatal stress (OPS) group exhibited down-regulation in both mRNA and protein expression of DNA methyltransferases (DNMT 3A and DNMT 3B), while up-regulation was observed in the expression of DNMT1. RRBS analyses identified ABCB1 and FKBP5 as hypermethylated genes, including a total of 43 differentially methylated sites (DMS) and 2 differentially methylated regions (DMR). MethylTarget™ sequencing further confirmed 15 differentially methylated CpG sites in these genes. This study provides preliminary evidence that PS disrupts the placental GC barrier through abnormal gene expression caused by hypermethylation of GC-related genes, resulting in elevated corticosterone levels in offspring and affecting their growth and development.
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Registered trials
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