Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Prenatal stress reprograms placental signaling and opposes maternal immune activation effects in the fetal brain

ABSTRACT: Prenatal psychosocial stress and maternal immune activation are associated with offspring psychiatric risk, but their effects on the placenta and fetal brain may involve shared or distinct transcriptional programs. This dataset profiles matched whole mouse placentas and whole fetal brains after prenatal restraint stress and a maternal poly(I:C) challenge. Placental bulk RNA-seq showed an attenuated antiviral transcriptional response to poly(I:C) after prenatal stress. Fetal-brain co-expression analyses identified overlapping DNA-repair, synaptic, and translational networks regulated in opposing directions by prenatal stress and maternal immune activation. Cross-tissue analyses assessed associations between placental antiviral gene-expression modules and fetal-brain networks.

ORGANISM(S): Mus musculus

PROVIDER: GSE347619 | GEO | 2026/09/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Maternal antioxidant treatment prevents the adverse effects of prenatal stress on the offspring's brain and behavior [NanoString nCounter rat miRNA]

Project description:Maternal exposure to stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. The mechanisms through which the effects of maternal stress are transmitted to the fetus are unclear, however the placenta, as the interface between mother and fetus, is likely to play a key role. Using a rat model, we investigated a role for placental oxidative stress in conveying the effects of maternal social stress to the fetus and the potential for treatment using a nanoparticle-bound antioxidant to prevent adverse outcomes in the offspring. Maternal psychosocial stress increased circulating corticosterone in the mother, but not in the fetuses. Maternal stress also induced oxidative stress in the placenta, but not in the fetal brain. Blocking oxidative stress using an antioxidant prevented the prenatal stress-induced anxiety phenotype in the male offspring, and prevented sex-specific neurobiological changes, specifically a reduction in dendrite lengths in the hippocampus, as well as reductions in the number of parvalbumin-positive neurons and GABA receptor subunits in the hippocampus and basolateral amygdala of the male offspring. Importantly, many of these effects were mimicked in neuronal cultures by application of placental-conditioned medium or fetal plasma from stressed pregnancies, indicating molecules released from the placenta may mediate the effects of prenatal stress on the fetal brain. Indeed, both placenta-conditioned medium and fetal plasma contained differentially abundant microRNAs following maternal stress, and their predicted targets were enriched for genes relevant to nervous system development and psychiatric disorders. The results highlight placental oxidative stress as a key mediator in transmitting the maternal social stress effects on the offspring's brain and behaviour, and offer a potential intervention to prevent stress-induced fetal programming of affective disorders.

2020-12-01 | GSE130573 | GEO

Prenatal stress reprograms placental signaling and opposes maternal immune activation effects in the fetal brain

Project description:Prenatal stress reprograms placental signaling and opposes maternal immune activation effects in the fetal brain

| PRJNA1530618 | ENA

Prenatal psychophysical and metabolic stress investigation on placenta tissue (MOMINFLAM)

Project description:Maternal stressors as psychophysical stress and obesity might share converging inflammatory/OS related pathways, disrupting fetal brain development, assuming a key role for the placenta in conveying maternal stressful mediators to the fetus. To test such hypothesis, we used two different mouse models mimicking, respectively, maternal psychophysical stress and maternal obesity and anlyased by LFQ-DIA mass spectrometry the placental tissue.

2023-07-10 | MSV000092388 | MassIVE

Neurodevelopmental Impact of Prenatal Stress: A Proteomic Analysis of Myelination Disruptions in the Avian Embryo

Project description:Prenatal stress induced by maternal activation of the hypothalamic-pituitary-adrenal (HPA) axis and subsequent release of glucocorticoids can profoundly affect fetal brain development. This study investigates the molecular mechanisms underlying prenatal stress in Gallus gallus domesticus by analyzing the brain proteome of embryos exposed to corticosterone. Using one of the most comprehensive proteomic analyses of the developing chicken brain to date, in which over 6,500 proteins were quantified, we identified significant myelination deficits as a key pathological feature. These results are consistent with previous research in mammalian models, highlighting the utility of Gallus gallus as a non-mammalian model for studying the effects of prenatal stress on neurodevelopment.

2025-10-27 | PXD055206 | Pride

Prenatal stress reprograms placental signaling and opposes maternal immune activation effects in the fetal brain [single-cell RNA-seq]

Project description:Prenatal stress reprograms placental signaling and opposes maternal immune activation effects in the fetal brain [single-cell RNA-seq]

| PRJNA1531029 | ENA

Prenatal Maternal Stress in Rats Alters the Epigenetic and Transcriptomic Landscape of the Maternal-Fetal Interface Across Four Generations [methylation]

Project description:Prenatal maternal stress (PNMS) determines lifetime mental and physical health. Here, we show in rats that PNMS has consequences for placental function and fetal brain development across four generations (F0-F3). Using a systems biology approach, comprehensive DNA methylation (DNAm), miRNA, and mRNA profiling revealed a moderate impact of PNMS in the F1 generation, but drastic changes in F2 and F3 generations, suggesting compounding effects of PNMS with each successive generation. Both maternal and placental miRNA gene targets included de novo DNA methyltransferases, indicating robust PNMS-induced disruption in the complex epigenetic regulatory network between miRNAs and DNAm. Transgenerational programming mainly involved genes and biological pathways associated with neurological and psychiatric diseases which were linked to maternal-fetal crosstalk facilitated by the placenta. The highly correlated placenta-brain profiles support the use of placenta as a noninvasive biomarker resource to predict pathological changes in the neonatal brain. The transgenerational persistence of critical DNAm, miRNA and mRNA signatures may explain familial non-genetic disease risks.

2024-10-07 | GSE276382 | GEO

Prenatal Maternal Stress in Rats Alters the Epigenetic and Transcriptomic Landscape of the Maternal-Fetal Interface Across Four Generations [miRNA]

2024-10-07 | GSE276226 | GEO

DNA hypermethylation in placental tissues: placental tissues vs. maternal peripheral bloods

Project description:Noninvasive prenatal diagnosis currently used does not achieve desirable levels of sensitivity and specificity. Recently, fetal methylated DNA biomarkers in maternal whole blood have been explored for noninvasive prenatal detection. However, such efforts cover only chromosomal aneuploidy; fetal methylated DNA biomarkers for detecting single-gene disease remain to be discovered. To address this issue, we systematically screened significantly hypermethylated genes in fetal tissues compared with maternal blood for noninvasive prenatal diagnosis of various inherited diseases. First, Methylated-CpG island recovery assay combined with CpG island array was performed in four maternal peripheral bloods and their corresponding placental tissues. Subsequently, direct bisulfite sequencing and combined bisulfite restriction analysis (COBRA) were carried out to validate the reliability of methylation microarray analysis. As results, 310 significantly hypermethylated genes in fetal tissues were detected by microarray. Two of five randomly selected hypermethylated genes detected by microarray were confirmed to be hypermethylated in fetal tissue samples by direct bisulfite sequencing. All four randomly selected hypermethylated genes detected by microarray were confirmed to be hypermethylated in five independent amniotic fluid samples and five independent chorionic villus samples from 10 pregnant women by CORBA. In conclusions, We found a lot of hypermethylated genes and methylation sites in fetal tissues, some of which have great potential to be developed into molecular markers for noninvasive prenatal diagnosis of monogenic disorders. Further clinical study is warranted to confirm these findings. Paired experiments, placental tissues vs. maternal peripheral bloods. Biological replicates: 4 placental tissues and 4 correspoding maternal peripheral bloods.

2012-02-22 | E-GEOD-35997 | biostudies-arrayexpress

HCMV infection mitigate the ability of placental EVs to potentiate neurogenesis by altering their miRNA landscape

Project description:Human cytomegalovirus (HCMV) is the most common virus transmitted in utero and a leading cause of infectious brain malformations and deafness, yet prognosis methods remain unreliable. Although certain central nervous system lesions caused by HCMV are explained, the neuropathogenesis of congenital infection remains poorly understood. The placenta, a key target of HCMV, plays a critical role during infection due to its involvement in maternal-fetal exchanges, particularly via the secretion of extracellular vesicles (EVs). Placental EVs mediate maternal-fetal communication, carrying proteins and RNAs, including microRNAs, that influence placental function, maternal immune tolerance, and viral defense. Our study explored the effects of placental EVs on fetal neural stem cell phenotype, demonstrating that EVs secreted from HCMV-infected placenta alter neurogenesis. Analysis of EV microRNA profiles revealed infection-induced alterations with predicted interference in brain development pathways. These findings highlight the critical role of placental EVs in fetal brain development and their contribution to HCMV neuropathogenesis.

2026-02-02 | PXD060921 | Pride

Impact of Maternal Immune Activation and Sex on Placental and Fetal Brain Cytokine and Gene Expression Profiles in a Preclinical Model of Neurodevelopmental Disorders

Project description:Maternal inflammation during gestation is associated with a later diagnosis of neurodevelopmental disorders including autism spectrum disorder (ASD). However, the specific impact of maternal immune activation (MIA) on placental and fetal brain development remains insufficiently understood. This study aimed to investigate the effects of MIA by analyzing placental and brain tissues obtained from the offspring of pregnant dams exposed to polyinosinic:polycytidylic acid (Poly I:C) on embryonic day 12.5. Cytokine and mRNA content in the placenta and brain tissues were assessed using multiplex cytokine assays and bulk-RNA sequencing on embryonic day 17.5. Bulk-RNA sequencing was performed on placenta and brain tissues on embryonic day 17.5.

2024-05-15 | GSE248222 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data