Genome-wide analysis of epigenomic alterations in fetal mouse forebrain after exposure to low doses of bisphenol A

Yaoi, Takeshi; Itoh, Kyoko; Nakamura, Keiko; Ogi, Hiroshi; Fujiwara, Yasuhiro; Fushiki, Shinji

doi:10.1016/j.bbrc.2008.09.028

Cited by 211 publications

(120 citation statements)

References 22 publications

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“…Finally, the findings of recent studies suggest that BPA appears to induce physiological responses such as DNA methylation via epigenetic mechanisms (Ho et al, 2006;Dolinoy et al, 2007;Yaoi et al, 2008;Baccarelli and Bollati, 2009;Bromer et al, 2010). Ho et al (2006) reported that neonatal exposure to BPA increases phosphodiesterase-4 expression, which results from early and increased DNA hypomethylation.…”

Section: Mechanisms Of Bpamentioning

confidence: 99%

“…Ho et al (2006) reported that neonatal exposure to BPA increases phosphodiesterase-4 expression, which results from early and increased DNA hypomethylation. Yaoi et al (2008) showed that exposure to low doses of BPA alters DNA methylation in the forebrain of a mouse fetus. Taken together, these findings suggest that although we cannot completely exclude the possibility of the estrogenic action of BPA, the action of BPA that is currently known may mainly be attributable to novel mechanisms underlying dopaminergic transmission.…”

Section: Mechanisms Of Bpamentioning

confidence: 99%

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Effects of Prenatal and Neonatal Exposure to Bisphenol A on the Development of the Central Nervous System

Mizuo¹,

Narita²,

Miyagawa³

et al. 2010

Biomolecules and Therapeutics

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-Bisphenol A (BPA) is one of the most common endocrine disrupters. In the last decade, the number of studies concerning the effects of chronic treatment with BPA on the development of the central nervous system (CNS) has increased. However, little is known about the effects of chronic exposure to BPA on higher brain functions such as memory or psychomotor functions. Here, we report our following findings: (1) Prenatal and neonatal exposure to BPA enhances psychostimulant-induced rewarding effects, results in the up-or downregulation of dopamine receptors, causes memory impairment, and decreases choline acetyltransferase (ChAT) activity. (2) BPA activates astrocytes in vivo and in vitro. These findings suggest that prenatal and neonatal exposure to BPA affects the development of the CNS.

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Section: Mechanisms Of Bpamentioning

confidence: 99%

Section: Mechanisms Of Bpamentioning

confidence: 99%

Effects of Prenatal and Neonatal Exposure to Bisphenol A on the Development of the Central Nervous System

Mizuo¹,

Narita²,

Miyagawa³

et al. 2010

Biomolecules and Therapeutics

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“…Several studies have linked gestational (13,14) or neonatal (15,16) BPA exposure to long-lasting changes in DNA methylation and altered gene expression in nonneuronal tissues. Investigation of the epigenetic effects of BPA in the brain has been very limited (17,18) and has not explored whether environmentally relevant doses of BPA could induce enduring effects on the brain epigenome. In addition, the dose-and sex-dependent effects of BPA have not been thoroughly examined, although they have been suggested by the loss of sexual dimorphism and sex-biased neurodevelopmental effects observed in animals and humans.…”

mentioning

confidence: 99%

Sex-specific epigenetic disruption and behavioral changes following low-dose in utero bisphenol A exposure

Kundaković

Gudsnuk

Franks

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

439

390

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Bisphenol A (BPA) is an estrogenic endocrine disruptor widely used in the production of plastics. Increasing evidence indicates that in utero BPA exposure affects sexual differentiation and behavior; however, the mechanisms underlying these effects are unknown. We hypothesized that BPA may disrupt epigenetic programming of gene expression in the brain. Here, we provide evidence that maternal exposure during pregnancy to environmentally relevant doses of BPA (2, 20, and 200 μg/kg/d) in mice induces sex-specific, dose-dependent (linear and curvilinear), and brain region-specific changes in expression of genes encoding estrogen receptors (ERs; ERα and ERβ) and estrogen-related receptor-γ in juvenile offspring. Concomitantly, BPA altered mRNA levels of epigenetic regulators DNA methyltransferase (DNMT) 1 and DNMT3A in the juvenile cortex and hypothalamus, paralleling changes in estrogen-related receptors. Importantly, changes in ERα and DNMT expression in the cortex (males) and hypothalamus (females) were associated with DNA methylation changes in the ERα gene. BPA exposure induced persistent, largely sex-specific effects on social and anxiety-like behavior, leading to disruption of sexually dimorphic behaviors. Although postnatal maternal care was altered in mothers treated with BPA during pregnancy, the effects of in utero BPA were not found to be mediated by maternal care. However, our data suggest that increased maternal care may partially attenuate the effects of in utero BPA on DNA methylation. Overall, we demonstrate that low-dose prenatal BPA exposure induces lasting epigenetic disruption in the brain that possibly underlie enduring effects of BPA on brain function and behavior, especially regarding sexually dimorphic phenotypes.environmental | fetal origin of adult disease

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“…51 Hormones are known regulators of transcription through their effect on DNA methylation and chromatin composition. 52,53 Since EDs can affect DNA methylation patterns 33,54,55 and gene expression, [56][57][58][59][60] it is hypothesized that these hormonelike chemicals can alter the reciprocal epigenetic states of the two parental chromosomes at imprinted genes or their DMRs and those epigenetic changes would alter the allele-specific expression in the embryonic or extraembryonic organs. To test this hypothesis we generated multiplex allele-specific assays and measured the effects of BPA, VZ and DEHP on the maintenance of imprinted gene expression of a representative set of imprinted transcripts in the embryo and in extraembryonic organs after in utero exposure to these chemicals.…”

Section: Effects Of Endocrine Disruptors On Imprinted Gene Expressionmentioning

confidence: 99%

Effects of endocrine disruptors on imprinted gene expression in the mouse embryo

Kang¹,

Iqbal²,

Tran³

et al. 2011

Epigenetics

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Genome-wide analysis of epigenomic alterations in fetal mouse forebrain after exposure to low doses of bisphenol A

Cited by 211 publications

References 22 publications

Effects of Prenatal and Neonatal Exposure to Bisphenol A on the Development of the Central Nervous System

Effects of Prenatal and Neonatal Exposure to Bisphenol A on the Development of the Central Nervous System

Sex-specific epigenetic disruption and behavioral changes following low-dose in utero bisphenol A exposure

Effects of endocrine disruptors on imprinted gene expression in the mouse embryo

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