Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE276382 | GEO | 2024/10/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

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 | GSE276226 | GEO

Maternal weight affects placental DNA methylation of genes invovled in metabolic pathways in the common marmoset monkey (Callithrix jacchus)

Project description:Accumulating evidence suggests that dysregulation of placental DNA methylation (DNAm) is a mechanism linking maternal weight during pregnancy to metabolic programming outcomes. The common marmoset, Callithrix jaccus, is a platyrrhine primate species that has provided much insight into studies of the primate placenta, maternal condition, and metabolic programming, yet the relationships between maternal weight and placental DNAm are unknown. Here, we report genome-wide DNAm from term marmoset placentas using reduced representation bisulfite sequencing. We identified 74 genes whose DNAm pattern is associated with maternal weight during gestation. These genes are predominantly involved in energy metabolism and homeostasis, including regulation of glycolytic and lipid metabolic processes pathways.

2020-01-07 | GSE143200 | GEO

Placental effects on maternal brain revealed by disrupted placental gene expression in mouse hybrids

Project description:The mammalian placenta is both the physical interface between mother and fetus, and the source of endocrine signals that target the maternal hypothalamus, priming females for parturition, lactation and motherhood. Despite the importance of this connection, the effects of altered placental signaling on the maternal brain are understudied. Here, we show that placental dysfunction alters gene expression in the maternal brain, with the potential to affect maternal behavior. Using a cross between the house mouse and the Algerian mouse in which hybrid placental development is abnormal, we sequenced late gestation placental and maternal medial preoptic area transcriptomes and quantified differential expression and placenta-maternal brain co-expression between normal and hybrid pregnancies. The expression of Fmn1, Drd3, Caln1 and Ctsr was significantly altered in the brains of females exposed to hybrid placentas. Most strikingly, expression patterns of placenta-specific gene families and Drd3 in the brains of house mouse females carrying hybrid litters matched those of female Algerian mice, the paternal species in the cross. Our results indicate that the paternally-derived placental genome can influence the expression of maternal-fetal communication genes, including placental hormones, suggesting an effect of the offspring's father on the mother’s brain.

2019-12-31 | GSE126469 | GEO

Maternal iron deficiency modulates placental transcriptome and proteome in mid-gestation of mouse pregnancy

Project description:Background: Maternal iron deficiency (ID) is associated with poor pregnancy and fetal outcomes. The effect is thought to be mediated by the placenta but there is no comprehensive assessment of placental response to maternal ID. Additionally, whether the influence of maternal ID on the placenta differs by fetal sex is unknown. Objectives: Our primary aim was to identify gene and protein signatures of ID mouse placentas at mid-gestation. A secondary objective was to profile the expression of iron genes in mouse placentas across gestation. Methods: We used a real-time PCR based array to determine the mRNA expression of all known iron genes in mouse placentas at embryonic day (E) 12.5, E14.5, E16.5, and E19.5 (n=3 placentas/time point). To determine the effect of maternal ID, we performed RNA sequencing and proteomics in male and female placentas from ID and iron adequate mice at E12.5 (n=8 dams/diet). Results: In female placentas, six genes including transferrin receptor (Tfrc) and solute carrier family 11 member 2 were significantly changed by maternal ID. An additional 154 genes were altered in male ID placentas. Proteomic analysis quantified 7662 proteins in the placenta. Proteins translated from iron responsive element (IRE) containing mRNAs were altered in abundance; ferritin and ferroportin 1 decreased while TFRC increased in ID placenta. Less than 4% of the significantly altered genes in ID placentas occurred both at the transcriptional and translational levels. Conclusions: Our data demonstrate that the impact of maternal ID on placental gene expression in mice is limited in scope and magnitude at mid-gestation. We provide strong evidence for IRE-based transcriptional and translational coordination of iron gene expression in the mouse placenta. Finally, we discover sexually dimorphic effects of maternal ID on placental gene expression, with more genes and pathways altered in male compared with female mouse placentas.

2021-03-12 | PXD023454 | Pride

microRNA sequencing of human placentae and matched maternal plasma from 6-23 weeks of gestation

Project description:microRNAs are increasingly seen as important regulators of placental development and opportunistic biomarker targets. We generated miRNA profiles using 96 placentas from presumed normal pregnancies, across early gestation, in combination with matched profiles from maternal plasma. We identified 637 miRNAs with expression in 86 samples (after removing poor quality samples), showing a clear gestational age gradient and identified 374 differentially expressed (DE) miRNAs across a gestational cut-off of 6-10 weeks’ and 11-23 weeks’. We see a clear gestational age group bias in miRNA clusters C19MC, C14MC, miR-17~92 and paralogs, regions that also include many DE miRNAs. Proportional change in expression of placenta-specific miRNA clusters was reflected in maternal plasma, with C19MC miRNAs miR-516b-5p and 517a-3p showing potential as a biomarkers. Chorionic villous samples across early gestation display differential miRNA profiles, particularly in the expression of highly placenta-specific miRNA clusters, and at the presumed introduction of oxygenated maternal blood into the placenta. Data presented here comprise a clinically important reference set for studying early placenta development and enabling development of minimally invasive methods for monitoring placental health.

2021-12-23 | GSE151362 | GEO

Mouse Placenta:Maternal experimental UTI vs Sham UTI infected

Project description:Transcriptional profiling to map the changes in placental function subsequent to maternal experimental UTI that result in intrauterine growth restriction. One condition experiment: 2 biological replicates of placenta from mice with maternal experimental UTI, 2 biological replicates of placenta from mice with sham UTI.

2011-09-09 | E-GEOD-32028 | biostudies-arrayexpress

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

miRNA levels in F1-F3 male germ cells and female F2 PFC following prenatal exposure to sGC in guinea pigs

Project description:Stress and glucocorticoid exposure during pregnancy alters neurodevelopment and behavior in offspring, and these effects extend multiple generations through a paternal lineage. The epigenetic mechanisms that govern this transgenerational transmission are unclear. We hypothesized that maternal exposure to multiple courses of sGC in late pregnancy would result in altered miRNA levels in germs cells of male guinea pigs across three generations. Further, our behavioral data indicate that F2 females exhibit altered behaviors following sGC exposure. Thus, we evaluated the miRNA profile of F2 female prefrontal cortex to determine the mechanisms responsible for these behavioral changes and to compare these data to our germ cell miRNA analysis. We used miRNA microarray to evaluate the miRNA levels in F1-F3 germ cells and F2 female PFC in guinea pigs that were exposed to control and F0 prenatal sGC exposure. We identified no significant changes to miRNA levels in both F1-F3 germ cells and F2 PFC from guinea pigs in the sGC group.

2024-01-25 | GSE250055 | GEO

Maternal pre-pregnancy obesity is associated with altered placental transcriptome

Project description:Maternal obesity is becoming a major health consideration for successful pregnancy outcomes. There is growing proof that maternal obesity has a negative influence on placental development and function, thereby adversely influencing offspring programming and health outcomes. However, the molecular mechanisms underlying these processes are so far poorly understood. We set out to analyse term placenta whole transcriptome in obese (n=5) and normoweight women (n=5), using Affymetrix microarray platform compromising of 50,000 probe sets. Our analysis shows that the placental transcriptome differs between normoweight and obese women. Different processes and pathways among placenta from obese women were dysregulated, including inflammation and immune responses, lipid metabolism, cell death and survival and cancer pathways, vasculogenesis and angiogenesis, and glucocorticoid receptor signaling pathway. Together, this global gene expression profiling approach demonstrates and confirms that maternal obesity creates a unique in utero environment that impairs placental transcriptome.

2017-01-07 | E-MTAB-4541 | biostudies-arrayexpress

Effect of Genetically Reduced Maternal Myostatin on Late Gestation Maternal, Fetal, and Placental Metabolomes in Mice.

Project description:Myostatin (gene symbol: Mstn) is an autocrine and paracrine inhibitor of muscle growth. Pregnant mice with genetically reduced levels of myostatin give birth to offspring with greater adult muscle mass and bone biomechanical strength. However, maternal myostatin is not detectable in fetal circulations. Fetal growth is dependent on the maternal environment, and the provisioning of nutrients and growth factors by the placenta. Thus, this study examined the effect of reduced maternal myostatin on maternal and fetal serum metabolomes, as well as the placental metabolome. Fetal and maternal serum metabolomes were highly distinct, which is consistent with the role of the placenta in creating a specific fetal nutrient environment. There was no effect from myostatin on maternal glucose tolerance or fasting insulin. In comparisons between pregnant control and Mstn+/- mice, there were more significantly different metabolite concentrations in fetal serum, at 50, than in the mother's serum at 33, confirming the effect of maternal myostatin reduction on the fetal metabolic milieu. Polyamines, lysophospholipids, fatty acid oxidation, and vitamin C, in fetal serum, were all affected by maternal myostatin reduction.

2023-06-08 | MTBLS3345 | MetaboLights

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