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Epigenetic profiling in adult brain after prenatal BPA exposure [RNA-seq]

ABSTRACT: Epigenetic profiling in adult brain after prenatal BPA exposure [RNA-seq]

PROVIDER: PRJNA1047018 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26993667.fastq.gz	Fastqsanger.gz
	SRR26993668.fastq.gz	Fastqsanger.gz
	SRR26993669.fastq.gz	Fastqsanger.gz
	SRR26993670.fastq.gz	Fastqsanger.gz
	SRR26993671.fastq.gz	Fastqsanger.gz

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Epigenetic profiling in adult brain after prenatal BPA exposure

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Epigenetic profiling in adult brain after prenatal BPA exposure [RRBS]

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Epigenetic profiling in adult brain after prenatal BPA exposure [ChIP-seq]

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Epigenetic profiling in adult brain after prenatal BPA exposure [ATAC-seq]

Project description:Epigenetic profiling in adult brain after prenatal BPA exposure [ATAC-seq]

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Epigenetic profiling in adult brain after prenatal BPA exposure [RRBS]

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

Epigenetic profiling in adult brain after prenatal BPA exposure [ATAC-seq]

2024-05-29 | GSE249015 | GEO

Epigenetic profiling in adult brain after prenatal BPA exposure [ChIP-seq]

2024-05-29 | GSE249014 | GEO

Epigenetic profiling in adult brain after prenatal BPA exposure [RNA-seq]

2024-05-29 | GSE249012 | GEO

Epigenetic profiling in adult brain after prenatal BPA exposure

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

2024-05-29 | GSE249016 | GEO

Effect of pubertal BPA exposure on mammary stem cells

Project description:Perinatal exposure to bisphenol A (BPA) has been shown to cause aberrant mammary gland morphogenesis and mammary neoplastic transformation. Yet, the underlying mechanism is poorly understood. We tested the hypothesis that mammary glands exposed to BPA during a susceptible window may lead to its susceptibility to tumorigenesis through a stem-cell mediated mechanism. We exposed 21-day-old Balb/c mice to BPA by gavage (25 µg/kg/day) during puberty for 3 weeks, and a subset of animals were further challenged with one oral dose (30 mg/kg) of 7,12-dimethylbenz[a]anthracene (DMBA) at 2 months of age. Primary mammary cells were isolated at 6 weeks, and 2 and 4 months of age for mammary stem cell (MaSC) quantification and function analysis. Pubertal exposure to the low-dose BPA increased lateral branches and hyperplasia in adult mammary glands and caused an acute increase of MaSC in 6-week-old glands and a delayed increase of luminal progenitors in 4-month-old adult gland. Most importantly, pubertal BPA exposure altered the function of MaSC from different age groups, causing pre-neoplastic lesions in their regenerated glands similar to those induced by DMBA exposure, which indicates that MaSCs are susceptible to BPA-induced transformation. Deep sequencing analysis on MaSC-enriched mammospheres identified a set of aberrantly expressed genes associated with pre-neoplastic lesions in human breast cancer patients. Thus, our study for the first time shows that pubertal BPA exposure altered MaSC gene expression and function such that they induced early neoplastic transformation.

2016-04-26 | GSE46815 | GEO

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