Genome-wide analysis of epigenomic alterations in fetal mouse forebrain after exposure to low doses of bisphenol A
Abstract
Bisphenol A (BPA) is one of endocrine disrupting chemicals, being distributed widely in the environment. We have been studying the low dose effects of BPA on murine forebrain development. Here, we have investigated the genome-wide effect of maternal exposure to BPA on the epigenome in mouse forebrain at E12.5 and at E14.5. We scanned CpG methylation status in 2500 NotI loci, representing 48 (de)methylated unique loci. Methylation status in most of them was primarily developmental stage-dependent. Each of almost all cloned NotI loci was located in a CpG island (CGI) adjacent to 5' end of the transcriptional unit. The mRNA expression of two functionally related genes changed with development as well as the exposure to BPA. In both genes, changes at the transcriptional level correlated well with the changes in NotI methylation status. Taken together, epigenetic alterations in promoter-associated CGIs after exposure to BPA may underlie some effects on brain development.
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In mice, BPA exposure alters the epigenomic profile of the fetal forebrain.
“In mice, BPA exposure has been shown to alter the epigenomic profile of the fetal forebrain (Yaoi et al., 2008).”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Yaoi et al., 2008
Epigenetic alterations have been implicated in BPA-associated changes in pathology and function in several hormone-responsive tissues including the brain.
“Epigenetic alterations have been implicated in BPA-associated changes in pathology and function in several hormone-responsive tissues including the brain [ 49 , 130 , 138–141 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [139]
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“In mice, BPA exposure has been shown to alter the epig-enomic profile of the fetal forebrain (Yaoi et al., 2008).”
- Authors
- Yaoi, T., Itoh, K., Nakamura, K., Ogi, H., Fujiwara, Y., & Fushiki, S.
- Affiliations
- Kyoto Prefectural University of Medicine (JP)
- Corresponding author
- Fushiki, Shinji
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2008-11
- Volume
- 376
- Issue
- 3
- Pages
- 563-567
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W2003636092
- Cited by
- 229
- References
- 23
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 5 · 2023: 7 · 2022: 6 · 2021: 6 · 2020: 9 · 2019: 11 · 2018: 8 · 2017: 18 · 2016: 16 · 2015: 22 · 2014: 21 · 2013: 19 · 2012: 30
- FWCI
- 6.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical and Biophysical Research Communications (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- bisphenol A, endocrine disruptors, maternal exposure, DNA methylation, CpG islands, promoter methylation, gene expression, low-dose exposure, mouse embryo
- MeSH terms
- Bisphenol A Compounds, Air Pollutants, Occupational, Animals, Benzhydryl Compounds, Estrogens, Non-Steroidal, Female, Fetus, Major Histocompatibility Complex, Mice, Inbred ICR, Phenols, Promoter Regions, Genetic, Proteins, Gene Expression, Prosencephalon, Genome, Maternal Exposure, CpG Islands, DNA Methylation, Genomics, Vesicular Transport Proteins, Epigenesis, Genetic, Mice
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