Gene expression in the mouse cerebral cortex exposed to Bisphenol A (BPA) during development.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE53158 | GEO | 2024/04/04
REPOSITORIES: GEO
Similar Datasets
Project description:In this study, developing zebrafish were exposed to 500-4500 µg/L BPA for 7 days from 3 hours post-fertilization for a microarray experiment to obtain molecular insights into BPA early-life exposure toxicity.
2012-06-01 | GSE22634 | GEO
Project description:In this study, developing zebrafish were exposed to 500-4500 µg/L BPA for 7 days from 3 hours post-fertilization for a microarray experiment to obtain molecular insights into BPA early-life exposure toxicity. We analyzed a total of 18 arrays; five biological replicate arrays for zebrafish treated with 500 µg/L BPA, four biological replicate arrays for zebrafish treated with 1500 µg/L BPA, four biological replicate arrays for zebrafish treated with 4500 µg/L BPA against 5 biological replicate arrays for control fish. A common reference sample was used for both treated and control samples.
2012-05-31 | E-GEOD-22634 | biostudies-arrayexpress
Project description:Environmental factors during perinatal development influence developmental plasticity and disease susceptibility via alterations to the epigenome. Developmental exposure to the endocrine active compound, bisphenol A (BPA), has previously been associated with altered methylation at candidate gene loci. Here, we undertake the first genome-wide characterization of DNA methylation profiles in the liver of murine offspring perinatally exposed to multiple doses of BPA through the maternal diet. Using a tiered focusing approach, our strategy proceeds from unbiased broad DNA methylation analysis using methylation-based next generation sequencing technology to in-depth quantitative site-specific CpG methylation determination using the Sequenom EpiTYPER MassARRAY platform to profile liver DNA methylation patterns in offspring maternally exposed to BPA during gestation and lactation to doses ranging from 0 BPA/kg (Ctr), 50 M-BM-5g BPA/kg (UG), or 50 mg BPA/kg (MG) diet (N=4 per group). Genome-wide analyses indicate non-monotonic effects of DNA methylation patterns following perinatal exposure to BPA, corroborating previous studies using multiple doses of BPA with non-monotonic outcomes. We observed enrichment of regions of altered methylation (RAMs) within CpG island (CGI) shores, but little evidence of RAM enrichment in CGIs. An analysis of promoter regions identified several hundred novel BPA-associated methylation events, and methylation alterations in the Myh7b and Slc22a12 gene promoters were validated. Using the Comparative Toxicogenomics Database, a number of candidate genes that have previously been associated with BPA-related gene expression changes were identified, and gene set enrichment testing identified epigenetically dysregulated pathways involved in metabolism and stimulus response. In this study, non-monotonic dose dependent alterations in DNA methylation among BPA-exposed mouse liver samples and their relevant pathways were identified and validated. The comprehensive methylome map presented here provides candidate loci underlying the role of early BPA exposure and later in life health and disease status. For this study, liver DNA from a subset of a/a wild-type animals was analyzed for full methylome characteristics: 1) standard diet (Ctr, n = 4 offspring; 2 male and 2 female); 2) 50 M-BM-5g BPA/kg diet (UG, n = 4 offspring; 2 male and 2 female); 3) 50 mg BPA/kg diet (MG, n = 4 offspring; 1 male and 3 female).
2013-11-17 | E-GEOD-46183 | biostudies-arrayexpress
Project description:Environmental factors during perinatal development influence developmental plasticity and disease susceptibility via alterations to the epigenome. Developmental exposure to the endocrine active compound, bisphenol A (BPA), has previously been associated with altered methylation at candidate gene loci. Here, we undertake the first genome-wide characterization of DNA methylation profiles in the liver of murine offspring perinatally exposed to multiple doses of BPA through the maternal diet. Using a tiered focusing approach, our strategy proceeds from unbiased broad DNA methylation analysis using methylation-based next generation sequencing technology to in-depth quantitative site-specific CpG methylation determination using the Sequenom EpiTYPER MassARRAY platform to profile liver DNA methylation patterns in offspring maternally exposed to BPA during gestation and lactation to doses ranging from 0 BPA/kg (Ctr), 50 µg BPA/kg (UG), or 50 mg BPA/kg (MG) diet (N=4 per group). Genome-wide analyses indicate non-monotonic effects of DNA methylation patterns following perinatal exposure to BPA, corroborating previous studies using multiple doses of BPA with non-monotonic outcomes. We observed enrichment of regions of altered methylation (RAMs) within CpG island (CGI) shores, but little evidence of RAM enrichment in CGIs. An analysis of promoter regions identified several hundred novel BPA-associated methylation events, and methylation alterations in the Myh7b and Slc22a12 gene promoters were validated. Using the Comparative Toxicogenomics Database, a number of candidate genes that have previously been associated with BPA-related gene expression changes were identified, and gene set enrichment testing identified epigenetically dysregulated pathways involved in metabolism and stimulus response. In this study, non-monotonic dose dependent alterations in DNA methylation among BPA-exposed mouse liver samples and their relevant pathways were identified and validated. The comprehensive methylome map presented here provides candidate loci underlying the role of early BPA exposure and later in life health and disease status.
2013-11-17 | GSE46183 | GEO
Project description:To elucidate the molecular perturbations underlying the connection of low-dose prenatal BPA exposure to cardiometabolic diseases, we assessed the liver transcriptome in both male and female mouse offspring exposed to 5ug/kg/day BPA and corn oil (control) during gestation.
2020-12-01 | GSE155845 | GEO
Project description:Purpose: finding differential transcripts usage in environmentally harzardous chemical, bisphenol A (BPA) in human retinal cells Methods: transcriptome analysis by the RNA-seq via mRNA pull-down Results: We found that BPA increases cellular toxicity by the increasing of early apoptotic pathway in Y79 cells. Also, over thounds of retained intron events were detected from the RNA-seq analysis. Conclusions: Bisphenol A (BPA) increases early cytotoxic effects in Y79 cells through the early apoptotic pathway and changes the context of trascript through the splicing regulation mechanisms.
2021-02-16 | GSE146255 | GEO
Project description:Bisphenol-A (BPA) is one of the most widespread endocrine disrupting chemicals (EDC) used as the base compound in the manufacture of polycarbonate plastics. Although evidence points to consider exposure to BPA as a risk factor for the development of Diabetes, its actions on whole body metabolism and on pancreatic beta cells are still unclear. The aim of this study was to study the in vivo effects of BPA on mice pancreatic islets, particularly on how it could regulate ion channels expression and function. And thus, bringing mechanistic insight into the suggested association between BPA exposure and health disorders. We used microarrays to detail the global profile of gene expression to identified different groups of up and down-regulated genes in the work model, with a special focus on genes related to ion channel-mediated actions of BPA in mice pancreatic β-cells.
2019-02-09 | GSE126297 | GEO
Project description:Endocrine disrupting compounds (EDCs) have the potential to cause adverse effects on wildlife and human health. Two important EDCs are the synthetic estrogen 17a-ethynylestradiol (EE2) and bisphenol A (BPA) both of which are xenoestrogens (XEs) as they bind the estrogen receptor and disrupt estrogen physiology in mammals and other vertebrates. In recent years the influence of XEs on oncogenes, specifically in relation to breast and prostate cancer has been the subject of considerable study. In this study healthy primary human prostate epithelial cells (PrECs) were exposed to environmentally relevant concentrations of BPA (5nM and 25nM BPA) and interrogated using a whole genome microarray. Microarray data were analyzed using the Pipeline for Integrated Microarray Expression and Normalization Toolkit (PIMENTo) that provides (1) data pre-processing, (2) and normalization to remove the technical variability across arrays data, (3) data visualization, (4) background subtraction, (5) quality control, and (6) differential expression (DE) analysis using the Bioconductor package 'limma'. Exposure to 5 and 25nM BPA generated 8,876 and 9,525 differentially expressed (DE) genes respectively in treated PrECs. Exposure to EE2 had the greatest effect on the PrEC transcriptome (2,389 DE genes) and all three exposures shared 7,011 common DE genes. Together, the low and high dose of BPA affected 1,839 genes not shared with the EE2 exposure.
2021-01-01 | E-MTAB-7576 | biostudies-arrayexpress
Project description:Gestational BPA exposure in sheep induces metabolic phenotype in sheep characterized by peripheral insulin resistance and increased adipocyte size. Because insulin sensitivity can be regulated by various agents including free fatty acids (FFA), we hypothesize that gestational BPA exposure alters circulating FFA inducing dyslipidemia, a marker of metabolic disorder. Because saturated FFA is associated with insulin resistance, determination of the FFA profile in these species aid in understanding the underlying mechanism. Additionally, because of the non-monotonic nature of responses to BPA exposure dose response studies are also needed. This study will therefore assess plasma lipid profile in sheep exposed to three different doses of BPA prenatally and compared with untreated control animals
2016-07-05 | ST000686 | MetabolomicsWorkbench
Project description:Aim: Identify Ambra1-dependent regulation in melanoma development by comparing bulk RNA extracted from Ambra1-depleted (BPA-/-) mouse melanomas to Ambra1-wt (BPA+/+) melanomas.
2021-03-04 | GSE151134 | GEO