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Maternal oxytocin treatment at birth increases epigenetic age in male offspring [array]

ABSTRACT: Maternal oxytocin treatment at birth increases epigenetic age in male offspring [array]

PROVIDER: PRJNA1005579 | ENA |

REPOSITORIES: ENA

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Maternal oxytocin treatment at birth increases epigenetic age in male offspring [array]

Project description:Rates of oxytocin use to induce or augment labor are increasing in the United States with little understanding of the impact on offspring development. Using a prairie vole animal model, we have shown that oxytocin administered to mothers can reach offspring brains with long lasting impacts on the development of social behaviors. Here, we examine the epigenetic and transcriptomic consequences of oxytocin exposure during birth in juvenile male offspring. First, we show that male offspring exposed to oxytocin at birth have increased epigenetic age compared to the saline exposed group. We also find 900 differentially methylated CpG sites (annotated to 589 genes), with 2 CpG sites (2 genes) remaining significant after correction for multiple comparisons. Differentially methylated CpG sites are involved in regulation of gene expression and neurodevelopment. Using RNA-sequencing we find 217 nominally differentially expressed genes (p<0.05) in nucleus accumbens, a brain region involved in reward circuitry and social behavior, including 6 genes that remain significantly differentially expressed after corrections for multiple comparisons. Finally, we show that maternal oxytocin administration leads to widespread alternative splicing in the nucleus accumbens. These results indicate that oxytocin exposure during birth has long lasting epigenetic consequences in the brain and warrant further investigation of how oxytocin administration impacts development and behavior throughout the lifespan.

2024-04-03 | GSE240833 | GEO

Maternal oxytocin treatment at birth increases epigenetic age in male offspring [RNA-seq]

2024-04-03 | GSE240832 | GEO

Maternal oxytocin treatment at birth increases epigenetic age in male offspring

Project description:Maternal oxytocin treatment at birth increases epigenetic age in male offspring

| PRJNA1005577 | ENA

Maternal oxytocin treatment at birth increases epigenetic age in male offspring [RNA-seq]

Project description:Maternal oxytocin treatment at birth increases epigenetic age in male offspring [RNA-seq]

| PRJNA1005323 | ENA

Transcriptomic changes in the medial prefrontal cortex of juvenile rat offspring after induced birth with oxytocin

Project description:We report changes in the medial prefrontal cortical transcriptome of male and female rat offspring after induced birth with oxytocin using RNA-seq analysis.

2023-04-05 | GSE228913 | GEO

Maternal oxytocin treatment at birth increases epigenetic age in male offspring

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-03 | GSE240856 | GEO

Transcriptomic changes in the medial prefrontal cortex of juvenile rat offspring after induced birth with oxytocin

Project description:Transcriptomic changes in the medial prefrontal cortex of juvenile rat offspring after induced birth with oxytocin

| PRJNA952158 | ENA

Maternal and offspring

Project description:Cecal microbiome of C-, WD- and REV-dams at weaning and in their offspring (C-offspring, WD-offspring, and REV-offspring, respectively) at 4 months.

| PRJEB64354 | ENA

Expression Data from Young Uteroplacental Insufficiency-induced Low Birth Weight Adult Guinea Pig Offspring

Project description:We aimed to gain mechanistic insights into the impact of uteroplacental insufficiency upon hepatic cholestrol metabolism pathways in young adult offspring.Uterine artery ablation-induced low birth weight (LBW) and normal birth weight (NBW) male and female guinea pig offspring were fed a control diet from weaning until postnatal day 150. Analysis of whole hepatic transcriptome results identified that between LBW and NBW offspring livers, 51 (29 up-regulated and 22 down-regulated) and 31 (8 up-regulated and 23 down-regulated) genes were differentially expressed in males and females respectively (fold change| >= 2 and p-value < 0.05). KEGG pathway analysis of these differentially expressed genes revealed that “Cholesterol metabolism” was an enriched pathway in LBW males but not females (p<0.05).

2020-11-10 | GSE161124 | GEO

Maternal multi-generational high fat diet (HFD) exposure increases the offspring HCC incidence

Project description:Purpose: To investiagte why maternal obesity induces the susceptibility of offspring to diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) over generations upon over nutrition.The goals of this study are to find over-generationally altered genes and miRNAs which may contribute the accumulative progeny susceptibility to HCC under over nutrition. Methods: C57BL/6 female mice (F0 generation) were fed with either normal chow (NC) or HFD (60% kcal fat) from 1-month to 3-month old, and mated with NC-fed male mice to produce F1 generation. The F2 generation was similarly created. Male offspring of the F0, F1 and F2 generations were intraperitoneally injected with DEN at 2-weeks-old, and kept inmaintained on HFD and named as H1D, H2D and H3D groups, respectively. Male offspring of the F0 generation injected with PBS (Nor group) or DEN (NCD group) at the same age and kept inmaintained on NC. All groups were sacrificed at 40-weeks-old. Liver mRNA profiles and miRNA profiles from the different offspring groups were generated by LncRNA sequencing and small RNA sequencing. Results: We identified many over-generationally changed genes and miRNAs in the offspring by RNA-sequencing. Conclusions: The study revealed an important role of miRNA and targeting genes in regulating the incidence of HCC in the offspring of maternal-lineage under multi-generational HFD exposure, which has a profound effect on exploring the link between maternal obesity and the development of diseases in offspring.

2021-07-01 | GSE117539 | GEO

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