Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fetal origin of sex-bias brain aging

ABSTRACT: DNA methylation plays crucial roles during fetal development as well as aging. Whether the aging of the brain is programmed at the fetal stage remains untested. To test this hypothesis, mouse epigenetic clock (epiclock) was profiled in fetal (gestation day 15), postnatal (day 5), and aging (week 70) brain of male and female C57BL/6J inbred mice. Data analysis showed that on week 70, the female brain was epigenetically younger than the male brain. Predictive modeling by neural network identified specific methylations in the brain at the developing stages that were predictive of epigenetic state of the brain during aging. Transcriptomic analysis showed coordinated changes in the expression of epiclock genes in the fetal brain relative to the placenta. Whole-genome bisulfite sequencing identified sites that were methylated both in the placenta and fetal brain in a sex-specific manner. Epiclock genes and genes associated with specific signaling pathways, primarily the gonadotropin-releasing hormone receptor (GnRHR) pathway, were associated with the sex-bias methylations in the placenta as well as the fetal brain. Transcriptional crosstalk among the epiclock and GnRHR pathway genes was evident in the placenta that was maintained in the brain during development as well as aging. Collectively, these findings suggest that sex differences in the aging of the brain are of fetal origin and epigenetically linked to the placenta.

ORGANISM(S): Mus musculus

PROVIDER: GSE157553 | GEO | 2022/08/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Fetal brain elicits sexually conflicting transcriptional response to the deficiency of uterine Forkhead Box A2 (Foxa2) in mice

Project description:RNA-seq identified different gene sets relating to biological functions such as aging, longevity, and nutrient sensing and signaling that were regulated in a sex-biased manner between the placenta and fetal brain. Conditional knockout of the transcription factor Forkhead Box A2 (Foxa2) in the uterus elicited sexual conflicting expression of those genes between the placenta and fetal brain.

2021-10-06 | GSE157555 | GEO

Role of Caveolin 1 in metabolic programming of fetal brain (bulk RNA-seq data)

Project description:Caveolae are plasma membrane invaginations found in most cells of mammals. Caveolin-1 (Cav1) encodes a major protein of the lipid rafts of these membrane structures. Cav1-null mice, though viable, show various phenotypic defects. At an early adult age, these mice show brain aging that resemble brain of one and half year old wildtype mice, and exhibit symptoms that are hallmarks of Alzheimer’s disease. It is not known if the ablation of Cav1 in these mice impacts the brain at the fetal stage that then influences brain function later in life. RNA-seq was performed to profile gene expression of fetal brain (gestation day 15) and aging brain (week 70) of Cav1 knockout mice. The data was comapred with genes expression data of fetal brain (gestation day 15) and aging brain (week 70) of wildtype mice from our earlier study.

2023-09-20 | GSE215139 | GEO

Fetal origin of sex-bias brain aging

Project description:Fetal origin of sex-bias brain aging

| PRJNA661735 | ENA

Fetal origin of sex-bias brain aging [RNA-seq]

Project description:In this study, gene expression of brain from postnatal (day 5) and aging (week 70) mice (C57BL/6J) was profiled. The data was used to infer transcriptional network of genes associated with epigenetic clock and GnRHR pathway in the brain. The results of this study suggested that brain aging originated early-in life.

2022-10-12 | GSE215138 | GEO

Fetal origin of sex-bias brain aging [RNA-seq]

Project description:Fetal origin of sex-bias brain aging [RNA-seq]

| PRJNA888983 | ENA

Placenta and fetal brain share a neurodevelopmental disorder DNA methylation profile in a mouse model of prenatal PCB exposure [WGBS]

Project description:Polychlorinated biphenyls (PCBs) are developmental neurotoxicants implicated as environmental risk factors for neurodevelopmental disorders (NDD). We examined the effects of prenatal exposure to a human-relevant mixture of PCBs on the DNA methylation profiles of fetal mouse brain and placenta. We found thousands of differentially methylated regions (DMRs) distinguishing placentas and brains from PCB-exposed embryos from sex-matched vehicle controls. In both placenta and brain, PCB-associated DMRs were enriched for functions related to neurodevelopment and cellular signaling and enriched within regions of bivalent chromatin. The placenta and brain PCB DMRs overlapped significantly and mapped to a shared subset of genes enriched for Wnt signaling, Slit/Robo signaling, and genes differentially expressed in NDD models. PBC DMRs also significantly overlapped with DMRs from the brains of humans with Rett syndrome and Dup15q syndrome. These results demonstrate that placenta can be used as a surrogate for embryonic brain DNA methylation changes relevant to an NDD.

2022-03-03 | GSE171016 | GEO

Placenta and fetal brain share a neurodevelopmental disorder DNA methylation profile in a mouse model of prenatal PCB exposure [RNA]

2022-03-03 | GSE171017 | GEO

Evidence for functional interactions between the placenta and brain in pregnant mice

Project description:In this study, we profiled gene expression of maternal brain, fetal brain and placenta at day 15 of pregnancy to investigate global crosstalk of genes between placenta and brain in mice .

2018-10-26 | GSE121799 | GEO

Female- and male-specific transcriptomic and epigenetic placental signatures in response to a maternal high fat diet in mice

Project description:Overnutrition during pregnancy inﬂuences the future health of the offspring, with outcomes differing depending on the child’s sex. The placenta is involved in the programming of obesity, type 2 diabetes and cardiovascular disease. Sex-specific adaptation of the placenta may be central to the differences in fetal growth and survival. The impact of diet and fetal sex on placental gene expression and epigenetic marks was investigated in mice fed a high-fat (HFD) or a control diet (CD), during the first 15 days of gestation Microarrays analysis revealed that expression was affected by maternal diet and was sexually dimorphic.

2012-04-01 | GSE29585 | GEO

Molecular Effects of Developmental FM 550 Exposure in Wistar Rat Fetal Forebrain

Project description:Firemaster® 550 (FM 550) is a flame retardant (FR) mixture that has become one of the most commonly used FRs in foam-based furniture and baby products. Human exposure to this commercial mixture, comprised of brominated and organophosphate components, is widespread. We have repeatedly shown that developmental exposure can lead to sex-specific behavioral effects in rats. Accruing evidence of endocrine disruption and potential neurotoxicity have raised concerns regarding the neurodevelopmental effects of FM 550 exposure, but the specific mechanisms of action remains unclear. Additionally, we observed significant, and in some cases sex-specific, accumulation of FM 550 in placental tissue following gestational exposure. Because the placenta is an important source of hormones and neurotransmitters for the developing brain, it may be a critical target of toxicity to consider in the context of developmental neurotoxicity. Using a mixture of targeted and exploratory approaches, the goal of the present study was to identify possible mechanisms of action in the developing forebrain and placenta. Wistar rat dams were orally exposed to FM 550 (0, 300, or 1,000 µg/day;) for 10 days during gestation and placenta and fetal forebrain tissue collected for analysis. In placenta, evidence of endocrine, inflammatory, and neurotransmitter signaling pathway disruption was identified. Notably, 5-HT turnover was reduced in placental tissue and fetal forebrains indicating that 5-HT signaling between the placenta and the embryonic brain may be disrupted. These findings demonstrate that environmental contaminants, like FM 550, have the potential to impact the developing brain by disrupting normal placental functions.

2018-02-28 | GSE108965 | 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