Epigenetic profiling in adult brain after prenatal BPA exposure [RRBS]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1047019 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Epigenetic profiling in adult brain after prenatal BPA exposure
| PRJNA1047014 | ENA
Project description:We reported that, in C57BL/6Slac mice, prenatally exposure to low-dose BPA induces up-regulation of genes associated with neuronal function and down-regulation of genes related to mitochondrial oxidative phosphorylation. Three-dimensional chromatin organization of these differential expressed genes revealed that up-regulated genes are primarily under control of remote enhancers, while down-regulated genes appear to be regulated by chromatin interactions among relative adjacent genes. Further examination of genome-wide repressive epigenetic modifications, specifically DNA methylation, H3K27me3, and H3K9me3 revealed that transcription of down-regulated genes might be repressed directly by enhanced DNA methylation and H3K27me3 modifications at promoter regions and indirectly by increased DNA methylation at their corresponding interaction regions, while up-regulated genes might be regulated by loss of H3K9me3 occupancy on distal regulatory regions.
2024-05-29 | GSE249013 | GEO
Project description:Epigenetic profiling in adult brain after prenatal BPA exposure [RNA-seq]
| PRJNA1047018 | ENA
Project description:Epigenetic profiling in adult brain after prenatal BPA exposure [ChIP-seq]
| PRJNA1047020 | ENA
Project description:Epigenetic profiling in adult brain after prenatal BPA exposure [ATAC-seq]
| PRJNA1047021 | ENA
Project description:The health impacts of endocrine disrupting chemicals (EDCs) remain debated and their tissue and molecular targets are poorly understood. Here, we leveraged systems biology approaches to assess the target tissues, molecular pathways, and gene regulatory networks associated with prenatal exposure to the model EDC Bisphenol A (BPA). Prenatal BPA exposure led to scores of transcriptomic and methylomic alterations in the adipose, hypothalamus, and liver tissues in mouse offspring, with cross-tissue perturbations in lipid metabolism as well as tissue-specific alterations in histone subunits, glucose metabolism and extracellular matrix. Network modeling prioritized main molecular targets of BPA, including Pparg, Hnf4a, Esr1, Srebf1, and Fasn. Lastly, integrative analyses identified the association of BPA molecular signatures with cardiometabolic phenotypes in mouse and human. Our multi-tissue, multi-omics investigation provides strong evidence that BPA perturbs diverse molecular networks in central and peripheral tissues, and offers insights into the molecular targets that link BPA to human cardiometabolic disorders.
2018-10-23 | GSE121604 | GEO
Project description:We reported that, in C57BL/6Slac mice, prenatally exposure to low-dose BPA induces up-regulation of genes associated with neuronal function and down-regulation of genes related to mitochondrial oxidative phosphorylation. Three-dimensional chromatin organization of these differential expressed genes revealed that up-regulated genes are primarily under control of remote enhancers, while down-regulated genes appear to be regulated by chromatin interactions among relative adjacent genes. Further examination of genome-wide repressive epigenetic modifications, specifically DNA methylation, H3K27me3, and H3K9me3 revealed that transcription of down-regulated genes might be repressed directly by enhanced DNA methylation and H3K27me3 modifications at promoter regions and indirectly by increased DNA methylation at their corresponding interaction regions, while up-regulated genes might be regulated by loss of H3K9me3 occupancy on distal regulatory regions.
2024-05-29 | GSE249015 | GEO
Project description:We reported that, in C57BL/6Slac mice, prenatally exposure to low-dose BPA induces up-regulation of genes associated with neuronal function and down-regulation of genes related to mitochondrial oxidative phosphorylation. Three-dimensional chromatin organization of these differential expressed genes revealed that up-regulated genes are primarily under control of remote enhancers, while down-regulated genes appear to be regulated by chromatin interactions among relative adjacent genes. Further examination of genome-wide repressive epigenetic modifications, specifically DNA methylation, H3K27me3, and H3K9me3 revealed that transcription of down-regulated genes might be repressed directly by enhanced DNA methylation and H3K27me3 modifications at promoter regions and indirectly by increased DNA methylation at their corresponding interaction regions, while up-regulated genes might be regulated by loss of H3K9me3 occupancy on distal regulatory regions.
2024-05-29 | GSE249014 | GEO
Project description:We reported that, in C57BL/6Slac mice, prenatally exposure to low-dose BPA induces up-regulation of genes associated with neuronal function and down-regulation of genes related to mitochondrial oxidative phosphorylation. Three-dimensional chromatin organization of these differential expressed genes revealed that up-regulated genes are primarily under control of remote enhancers, while down-regulated genes appear to be regulated by chromatin interactions among relative adjacent genes. Further examination of genome-wide repressive epigenetic modifications, specifically DNA methylation, H3K27me3, and H3K9me3 revealed that transcription of down-regulated genes might be repressed directly by enhanced DNA methylation and H3K27me3 modifications at promoter regions and indirectly by increased DNA methylation at their corresponding interaction regions, while up-regulated genes might be regulated by loss of H3K9me3 occupancy on distal regulatory regions.
2024-05-29 | GSE249012 | GEO
Project description:In this study, we investigated the prenatal effects of bisphenol-A (BPA) exposure on transcriptome profiles in the hippocampus of the rat offspring. Transcriptome profiling by RNA-seq analysis of hippocampi isolated from neonatal pups prenatally exposed to BPA was conducted and revealed a list of differentially expressed genes (DEGs) associated with ASD. Among the DEGs, several ASD candidate genes, including Auts2 and Foxp2, were dysregulated and showed sex differences in response to BPA exposure. The interactome and pathway analyses of DEGs revealed significant associations between the DEGs in males and neurological functions/disorders associated with ASD. The findings from this study indicate that prenatal BPA exposure alters the expression of ASD-linked genes in the hippocampus and suggest that maternal BPA exposure may increase ASD susceptibility by dysregulating genes associated with neurological functions known to be negatively impacted in ASD.
2019-11-14 | GSE140298 | GEO