Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic Disruptions in the Offspring Hypothalamus in Response to Maternal Infection

ABSTRACT: Epigenetic Disruptions in the Offspring Hypothalamus in Response to Maternal Infection

PROVIDER: PRJNA1053359 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27227866.fastq.gz	Fastqsanger.gz
	SRR27227867.fastq.gz	Fastqsanger.gz
	SRR27227868.fastq.gz	Fastqsanger.gz
	SRR27227869.fastq.gz	Fastqsanger.gz
	SRR27227870.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Epigenetic disruptions in the offspring hypothalamus in response to maternal infection.

Project description:DNA methylation is an epigenetic modification that can alter gene expression, and the incidence can vary across developmental stages, inflammatory conditions, and sexes. The effects of viral maternal viral infection and sex on the DNA methylation patterns were studied in the hypothalamus of a pig model of immune activation during development. DNA methylation at single-base resolution in regions of high CpG density was measured on 24 individual hypothalamus samples using reduced representation bisulfite sequencing. Differential over- and under-methylated sites were identified and annotated to proximal genes and corresponding biological processes. A total of 120 sites were differentially methylated (FDR-adjusted p-value < 0.05) between maternal infection or sex groups. Among the 66 sites differentially methylated between groups exposed to inflammatory signals and control, most sites were over-methylated in the challenged group and included sites in the promoter regions of genes SIRT3 and NRBP1. Among the 54 differentially methylated sites between females and males, most sites were over-methylated in females and included sites in the promoter region of genes TNC and EIF4G1. The analysis of the genes proximal to the differentially methylated sites suggested that biological processes potentially impacted include immune response, neuron migration and ensheathment, peptide signaling, adaptive thermogenesis, and tissue development. These results suggest that translational studies should consider that the prolonged effect of maternal infection during gestation may be enacted through epigenetic regulatory mechanisms that may differ between sexes.

| S-EPMC11826927 | biostudies-literature

Maternal dietary fat during lactation shapes single nucleus transcriptomic profile of postnatal offspring hypothalamus in a sexually dimorphic manner in mice

Project description:Maternal overnutrition during pregnancy/or lactation predisposes offspring obesity and related metabolic syndromes in later life. Hypothalamus is the highest heterogeneous brain region located at the base of the brain that is critical to the regulation of the energy homeostasis.We investigated how the maternal programming shapes the single-nucleus transcriptomic landscapes in postnatal day15 offspring hypothalamus in a sex-specific manner.

2024-02-18 | GSE217677 | GEO

Maternal obesity alters neurotrophin-associated MAPK ignaling in the hypothalamus of male mouse offspring

Project description:In the present project we examined the effects of maternal obesity to offspring hypothalamic tissue at postnatal day (P) 21. Maternal obesity has emerged as an important risk factor for the development of metabolic disorders in the offspring.To obtain an overview of affected genes in the offsprings hypothalamus, the center of hunger and satiety in the brain, we performed whole genome microarray expression profiling. Female mice were fed either a control diet (SD) or a high fat diet (HFD) after weaning until mating and during pregnancy and gestation. On P21, male pups were sacrificed and blood samples were collected for further analyses. The hypothalamus was cut immediately caudal to the optic chiasm. The dissection was limited laterally by the hypothalamic sulci and dorsally by the mammillothalamic tract. Hypothalamic tissue was immediately frozen at −80° C. A maximum of two offspring per dam were analysed to minimize litter-dependent bias. All studies were performed using male offspring.

2019-08-15 | GSE135830 | GEO

Epigenetic Disruptions in the Offspring Hypothalamus in Response to Maternal Infection

Project description:Female and male 21 days of age pigs were studied. Half of the pigs were prenatally exposed to immune activation from virally-infected gilts, and half were not exposed.

2025-02-19 | GSE250318 | GEO

Changes in miRNA expression in offspring hypothalamus after exposure to maternal obesity

Project description:Changes in miRNA expression in offspring hypothalamus after exposure to maternal obesity

| PRJNA1086988 | ENA

Changes in miRNA expression in offspring hypothalamus after exposure to maternal obesity

Project description:The purpose of this study was to identify miRNA that are differentially regulated in the arcuate nucleus of the hypothaamus (ARC) and paraventricular nucleus of the hypothalamus (PVH) after perinatal exposure to maternal obesity.

2024-03-13 | GSE261455 | GEO

Hypothalamus transcriptome signatures underlying metabolic malprogramming in offspring mice exposed to a maternal obesogenic environment

Project description:Purpose: Identify the potential effector that might responding to the irritated hypothalamic ER stress as early as postnatal resulting from maternal obesity exposure. Methods: Three-week-old male offspring were selected for extracting RNA sample from the three groups (triplicate in sample): LP (Lg42_P1, Lg63_P2, Lg63_P3), HP (Hg43_P1, Hg43_P2, Hg13_P3) and HA (Hg43_A1, Hg43_A2, Hg13_A3). After standard RNA quantification and qualification, library preparation, clustering, sequencing and quality control, reads were mapped to the reference genome, and quantified of gene expression level with FPKM. The data were further processed for differential expression and other functional analysis. Results: We identified 789 differentially expressed genes (DEGs) (DESeq2, pvalue<0.05, |log2FoldChange|>0.0) in the mice from HP compared with those from LP, of which 408 (52%) were upregulated, while 381 (48%) downregulated. Whereas, for those of HA versus HP, 726 DEGs were detected, with 401 (55%) upregulated and 325 (45%) downregulated. There was a total of 158 overlapped DEGs between the two compared groups. In the following Gene Ontology enrichment analysis, we found that the upregulated DEGs in the HP group were significantly enriched in the categories related to molecular chaperon mediated protein processing. While for those downregulated DEGs in HA, similar theme was enriched with most of the genes from family members of the heat shock protein (Hsp), especially Hsp70. We validated the alteration of two members of Hsp70 in the hypothalamus of the weaning offspring given their crucial role in the stress response. Conclusions: Hspa1b might be the potential effector for the irritated early hypothalamic ER stress and the root of unbalanced stress balance in the hypothalamus undergoing feeding-related circuit axon projection in male offspring from obese dams.

2021-03-05 | GSE162744 | GEO

Maternal high fat diet induces circadian clock-independent endocrine alterations impacting metabolism of the offspring

Project description:Maternal obesity has long-term effects on offspring metabolic health. Among the potential mechanisms, prior research has indicated potential disruptions in circadian rhythms and gut microbiota in the offspring. To challenge this hypothesis, we implemented a maternal high fat diet regimen before and during pregnancy, followed by a standard diet after birth. Our findings confirm that maternal obesity impacts offspring birth weight and glucose and lipid metabolisms. However, we found minimal impact on circadian rhythms and microbiota that are predominantly driven by the feeding/fasting cycle. Notably, maternal obesity altered rhythmic liver gene expression, affecting mitochondrial function and inflammatory response without disrupting the hepatic circadian clock. These changes could be explained by a masculinisation of liver gene expression similar to the changes observed in polycystic ovarian syndrome. Intriguingly, such alterations seem to provide the first-generation offspring with a degree of protection against obesity when exposed to a high fat diet.

2024-06-09 | GSE240147 | GEO

Maternal slimming reprograms metabolic gene expression in mice offspring

Project description:This SuperSeries is composed of the following subset Series: GSE40471: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen expression) GSE40477: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen methylation) GSE40478: Maternal slimming reprograms metabolic gene expression in mice offspring (mRNA-Seq) Refer to individual Series

2012-08-30 | E-GEOD-40479 | biostudies-arrayexpress

DNA Methylation profile in hypothalamus for mouse offspring with maternal high fat (HF), low protein (LP) and control (CO) diets

Project description:To investigate the materal dietary effects (HF, LP) on affecting DNA methylations in the mouse offspring hypothalamus.

2019-01-01 | GSE79619 | GEO