Mus musculus
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ABSTRACT:
PROVIDER: PRJNA343002 | ENA |
REPOSITORIES: ENA
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Project description:Preferential Epigenetic Programming of Estrogen Response after in utero xenoestrogen (bisphenol-A) exposure
| PRJNA350333 | ENA
Project description:Preferential Epigenetic Programming of Estrogen Response after in utero xenoestrogen (bisphenol-A) exposure [NimbleGen]
| PRJNA350332 | ENA
Project description:Bisphenol-A (BPA) is an environmentally ubiquitous estrogen-like endocrine-disrupting compound. Exposure toBPAin utero hasbeen linked tofemale reproductive disorders, including endometrial hyperplasiaandbreast cancer. Estrogens are an etiological factor in many of these conditions. We sought to determine whether in utero exposure to BPA altered the globalCpGmethylation pattern of the uterine genome, subsequent gene expression, and estrogen response.Pregnantmicewere exposed to an environmentally relevant dose of BPAorDMSOcontrol.Uterine DNAand RNAwere examined by usingmethylatedDNAimmunoprecipitationmethylation microarray, expression microarray, and quantitative PCR. In utero BPA exposure altered the global CpG methylation profile of the uterine genome and subsequent gene expression. The effect on gene expression was not apparent until sexual maturation, which suggested that estrogen response was the primary alteration. Indeed, prenatal BPA exposure preferentially altered adult estrogen-responsive gene expression. Changes in estrogen response were accompanied by altered methylation that preferentially affected estrogen receptor-a (ERa)–binding genes. The majority of genes that demonstrated both altered expression and ERa binding had decreased methylation. BPA selectively altered the normal developmental programming of estrogen-responsive genes via modification of the genes that bind ERa. Gene– environment interactions driven by early life xenoestrogen exposure likely contributes to increased risk of estrogenrelateddisease in adults.—Jorgensen, E. M.,Alderman,M.H., III,Taylor, H. S. Preferential epigenetic programmingof estrogen response after in utero xenoestrogen (bisphenol-A) exposure.
2016-10-24 | GSE89125 | GEO
Project description:Bisphenol-A (BPA) is an environmentally ubiquitous estrogen-like endocrine-disrupting compound. Exposure toBPAin utero hasbeen linked to female reproductive disorders, including endometrial hyperplasia and breast cancer. Estrogens are an etiological factor in many of these conditions. We sought to determine whether in utero exposure to BPA altered the global CpG methylation pattern of the uterine genome, subsequent gene expression, and estrogen response. Pregnant mice were exposed to an environmentally relevant dose of BPA or DMSO control. Uterine DNA and RNA were examined by using methylated DNA immunoprecipitation methylation microarray, expression microarray, and quantitative PCR. In utero BPA exposure altered the global CpG methylation profile of the uterine genome and subsequent gene expression. The effect on gene expression was not apparent until sexual maturation, which suggested that estrogen response was the primary alteration. Indeed, prenatal BPA exposure preferentially altered adult estrogen-responsive gene expression. Changes in estrogen response were accompanied by altered methylation that preferentially affected estrogen receptor-a (ERa)–binding genes. The majority of genes that demonstrated both altered expression and ERa binding had decreased methylation. BPA selectively altered the normal developmental programming of estrogen-responsive genes via modification of the genes that bind ERa. Gene– environment interactions driven by early life xenoestrogen exposure likely contributes to increased risk of estrogen related disease in adults.—Jorgensen, E. M.,Alderman,M.H., III,Taylor, H. S. Preferential epigenetic programmingof estrogen response after in utero xenoestrogen (bisphenol-A) exposure.
2016-09-15 | GSE86923 | GEO
Project description:Bisphenol-A is a widespread endocrine disruptor chemical. In utero or perinatal exposure to bisphenol-A (BPA), leads to impaired glucose metabolism during adulthood. To investigate the consequences of the exposure to bisphenol-A during development in pancreatic beta-cell growth We used microarrays to determine gene expression changes resulting from exposure to bisphenol-A during pregnancy in pancreatic islets of the male offspring at postnatal day 30.
2017-06-01 | GSE82175 | GEO
Project description:Estrogens regulate many reproductive processes in fish and other vertebrates. In fish, the pituitary and liver are among the main sites of action of estrogens in the reproductive brain-pituitary-gonadal-hepatic axis. Environmental contaminants with estrogenic compounds acting at these organs have the potential to interfere with the reproductive processes in fish. In this work, RNA-seq analysis was performed to map estrogen and xenoestrogen target genes in the juvenile female Atlantic cod (Gadus morhua) liver after 72 h exposure to estrogenic compounds ethynylestradiol (EE2), and the xenoestrogens bisphenol A (BPA) and methoxychlor (MXC). Our results show that, in the liver, EE2 and the xenoestrogens modulated many genes and pathways related to vitellogenesis and lipid metabolism.
2025-12-31 | E-MTAB-12604 | biostudies-arrayexpress
Project description:MCF7 cells were exposed to xenoestrogens (vehicle = 0.1% ethanol, 30 pM 17beta-estradiol, 3 micromolar genistein, 10 micromolar genistein, 1 micomolar daidzein, 10 nM bisphenol A, 10 nM para-nonylphenol, 3 nM PPT) for 48 hours. Keywords: xenoestrogen response
2006-07-01 | GSE5200 | GEO
Project description:Background: Environmental exposures co-occurring during early life have a profound influence on neurodevelopment. Our previous work in rats suggests that postnatal maternal care modulates the effects of prenatal exposure to bisphenols, an estrogenic endocrine disrupting chemical, on offspring neurodevelopment. Elevated postnatal maternal licking/grooming and prenatal bisphenol exposure have known opposing effects on estrogen receptor alpha (Esr1) expression in the medial preoptic area (MPOA) of the hypothalamus, which could impact expression of estrogen-responsive genes. Based on this previous work, we hypothesized that postnatal maternal licking/grooming would mitigate the effects of prenatal bisphenol exposure on Esr1 expression and estrogen-responsive genes in the developing MPOA. In addition, we hypothesized that there would be interactive effects of prenatal bisphenol exposure and postnatal maternal licking/grooming on DNA methylation, particularly nearby estrogen responsive elements. Results: Our results indicated a significant interaction between prenatal bisphenol exposure and maternal postnatal licking/grooming on estrogen-related receptor gamma (Esrrg) expression in female pups. These interactions were also evident in co-expression gene profiles in female pups; the majority of which were enriched for estrogen-responsive genes. Finally, DNA methylation analyses indicated that adding postnatal maternal licking/grooming as a covariate influenced the number of differentially methylated regions for prenatal bisphenol-exposed male and female pups. These differentially methylated regions were enriched for binding sites for transcription factors that are known to interact with estrogen receptors, suggesting some secondary effects on postnatal gene regulation. Conclusions: These results suggest a novel biological mechanism in which postnatal maternal care can mitigate the negative neurodevelopmental impacts of prenatal bisphenol exposure.
2025-11-21 | GSE310190 | GEO
Project description:Background: Environmental exposures co-occurring during early life have a profound influence on neurodevelopment. Our previous work in rats suggests that postnatal maternal care modulates the effects of prenatal exposure to bisphenols, an estrogenic endocrine disrupting chemical, on offspring neurodevelopment. Elevated postnatal maternal licking/grooming and prenatal bisphenol exposure have known opposing effects on estrogen receptor alpha (Esr1) expression in the medial preoptic area (MPOA) of the hypothalamus, which could impact expression of estrogen-responsive genes. Based on this previous work, we hypothesized that postnatal maternal licking/grooming would mitigate the effects of prenatal bisphenol exposure on Esr1 expression and estrogen-responsive genes in the developing MPOA. In addition, we hypothesized that there would be interactive effects of prenatal bisphenol exposure and postnatal maternal licking/grooming on DNA methylation, particularly nearby estrogen responsive elements. Results: Our results indicated a significant interaction between prenatal bisphenol exposure and maternal postnatal licking/grooming on estrogen-related receptor gamma (Esrrg) expression in female pups. These interactions were also evident in co-expression gene profiles in female pups; the majority of which were enriched for estrogen-responsive genes. Finally, DNA methylation analyses indicated that adding postnatal maternal licking/grooming as a covariate influenced the number of differentially methylated regions for prenatal bisphenol-exposed male and female pups. These differentially methylated regions were enriched for binding sites for transcription factors that are known to interact with estrogen receptors, suggesting some secondary effects on postnatal gene regulation. Conclusions: These results suggest a novel biological mechanism in which postnatal maternal care can mitigate the negative neurodevelopmental impacts of prenatal bisphenol exposure.
2025-11-21 | GSE310191 | GEO
Project description:Estrogens regulate many reproductive processes in fish and other vertebrates. In fish, the pituitary and liver are among the main sites of action of estrogens in the reproductive brain-pituitary-gonadal-hepatic axis. Environmental contaminants with estrogenic compounds acting at these organs have the potential to interfere with the reproductive processes in fish. In this work, RNA-seq analysis was performed to map estrogen and xenoestrogen target genes in the juvenile female Atlantic cod (Gadus morhua) after 72 h exposure to estrogenic compounds ethynylestradiol (EE2), and the xenoestrogens bisphenol A (BPA) and methoxychlor (MXC). Our results show that, in the pituitary, EE2 and the xenoestrogens modulated many genes and pathways related to reproduction (such as hormone synthesis, hormonal signaling), metabolic homeostasis, and cell differentiation and proliferation. The xenoestrogens BPA and MXC had similar effect as EE2 on the top differentially expressed genes, suggesting their potential to disrupt pituitary functions.
2025-12-31 | E-MTAB-12762 | biostudies-arrayexpress