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E-GEOD-58516

ABSTRACT: Gene expression profile of adipocytes treated with bisphenol A or 17beta-estradiol

OTHER RELATED OMICS DATASETS IN: PRJNA252814

PROVIDER: E-GEOD-58516 | ExpressionAtlas | 2015-09-18

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-58516-analysis-methods.tsv	Tabular
	E-GEOD-58516-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-58516-configuration.xml	Xml
	E-GEOD-58516-percentile-ranks.tsv	Tabular
	E-GEOD-58516.condensed-sdrf.tsv	Tabular

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High content analysis of estrogen receptor activity: a mechanism-driven approach to compound testing

Project description:Analysis of the genome-wide response of the ER:PRL-HeLa cell line to treatment with estrogen receptor ligands estradiol, 4H-tamoxifen and bisphenol-A. Total RNA obtained from ER:PRL-HeLa cells treated for 4 hours with estradiol, 4H-tamoxifen or bisphenol -A is compared to vehicle treated controls

2011-07-13 | E-GEOD-22941 | biostudies-arrayexpress

Effects of bisphenol A on gene expression in adipocytes from lean children: association to metabolic disorders

Project description:Bisphenol A (BPA) is a xenobiotic endocrine disrupting chemical. In vitro and in vivo studies indicated that BPA alters endocrine-metabolic pathways in adipose tissue increasing the risk of developing metabolic disorders. BPA effects on human adipocytes, specifically in children, are poorly investigated. To investigate in childhood the effect of exposure to BPA on metabolic disorders we analyzed in vitro the effects of environmentally relevant doses of BPA on gene expression of mature human adipocytes from pre-pubertal lean patients and on related physiological outcomes. Adipocytes from children were treated in vitro with BPA and gene expression was evaluated by qRT-PCR. Genome wide analyses were performed using GeneChip Human Gene 1.0 ST array. Lipid content in adipocytes was estimated by ORO staining and Triglyceride Quantification Kit. Secreted IL-1beta, in adipocytes culture medium, and insulin, in PANC-1 culture medium, were performed using ELISA assays. BPA was found to promote up-regulation of ER? and ERR?, and down-regulation of GPR30 expression modulating estrogen signaling and following a non-linear dose-response. Microarray data analysis demonstrated that BPA increases the gene expression of pro-inflammatory cytokines and lipid metabolism-related FABP4 and CD36 in adipocytes. PCSK1 resulted the most interesting gene being down-regulated by BPA thus impairing insulin production in pancreas. BPA promotes inflammation and lipid metabolism dysregulation in adipocytes from lean children. Moreover, PCSK1 can be a key gene in BPA action modulating insulin production. Exposure to BPA in childhood may be an important risk factor in developing obesity and metabolic disorders. Three prototypic situations were analyzed (5 replication each): untreated cells (C), 10 nM BPA treated cells (BPA), 1 nM 17-beta Estradiol treated cells (ES).

2015-07-09 | E-GEOD-58516 | biostudies-arrayexpress

Comparative analysis of transcriptomic changes induced by zearalenone and bisphenol A in human ovarian cancer cells [mRNA_seq]

Project description:In this study we compared the global transcriptomic response of human ovarian cells to zeralenone (ZEA; mycotoxin) and bisphenol A (BPA; plastic additive) with the effect of physiological estradiol (E2). For this purpose we applied the PEO1 human ovarian cell line that was treated with 10 nM ZEA, 100 nM BPA and 10 nM E2. Transcriptomic profile was compared by mRNA sequencing (Illumina NextSeq 500).

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Comparative analysis of transcriptomic changes induced by zearalenone and bisphenol A in human ovarian cancer cells [microRNA_seq]

Project description:In this study we compared the effect of zeralenone (ZEA; mycotoxin) and bisphenol A (BPA; plastic additive) to the global microRNA expression of human ovarian cells with the effect of physiological estradiol (E2). For this purpose we applied the PEO1 human ovarian cell line that was treated with 10 nM ZEA, 100 nM BPA and 10 nM E2. MicroRNA expression was compared by microRNA sequencing (Illumina NextSeq 500).

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The effect of bisphenol A on human prostaspheres derived from primary prostate epithelial cells

Project description:Bisphenol A is an environmental xenoestrogen commonly known as an endocrine disruptor. We previously reported BPA-treated human primary prostate epithelial cell derived prostaspheres had larger size, exhibited clonogenicity, and showed increase in stem cell marker expression. Results reveal the molecular basis of BPA action in human prostate stem-progenitor cells. Human primary prostate epithelial cells from three disease-free Caucasian donors formed prostaspheres from single stem-like cells in matrigel cultures and were treated with 0.1 nM estradiol-17β (E2), 10 nM (B10), 200 nM (B200), and 1000 nM bisphenol A (BPA) for 7 days. The vehicle-treated prostaspheres were used as 'untreated controls'.

2014-11-05 | E-GEOD-62953 | biostudies-arrayexpress

Expression Analysis of Bisphenol A (0.1 uM), 17beta-estradiol (0.1 uM), and GSK4716 (0.1 uM) Exposure in Embryonic Zebrafish

Project description:Investigation of whole genome expression pattern of 24 hours post fertilization Danio rerio embryos exposed to bisphenol A, 17beta-estradiol, GSK4716, or 0.1% DMSO vehicle control

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2024-03-15 | PXD050702 |

High content analysis of estrogen receptor activity: a mechanism-driven approach to compound testing

Project description:Analysis of the genome-wide response of the ER:PRL-HeLa cell line to treatment with estrogen receptor ligands estradiol, 4H-tamoxifen and bisphenol-A.

2011-07-14 | GSE22941 | GEO

Genistein and bisphenol A exposure cause estrogen receptor 1 to bind thousands of binding sites in a cell type-specific manner

Project description:To obtain an integrated view of gene regulation in response to environmental and endogenous estrogens on a genome-wide scale, we performed ChIP-seq, to identify estrogen receptor 1 (ER) binding sites, and RNA-seq in endometrial cancer cells exposed to bisphenol A (BPA; found in plastics), genistein (GEN; found in soybean), or 17β-estradiol (E2; an endogenous estrogen). GEN and BPA treatment induces thousands of ER binding sites and >50 gene expression changes, representing a subset of E2‑induced gene regulation changes. Genes affected by E2 were highly enriched for ribosome-associated proteins; however, GEN and BPA failed to regulate most ribosome-associated proteins and instead enriched for transporters of carboxylic acids. Treatment-dependent changes in gene expression were associated with treatment-dependent ER binding sites, with the exception that many genes up-regulated by E2 harbored a BPA-induced ER binding site, but failed to show any expression change after BPA treatment. GEN and BPA exhibited a similar relationship to E2 in the breast cancer line T-47D, where cell type specificity played a much larger role than treatment specificity. Overall, both environmental estrogens clearly regulate gene expression through ER on a genome-wide scale, although with lower potency resulting in less ER binding sites and less gene expression changes compared to the endogenous estrogen, E2. RNA-seq of human cancer cell lines treated with estradiol, bisphenol A, genistein or DMSO (control)

2012-06-13 | E-GEOD-38234 | biostudies-arrayexpress

Effects of bisphenol A on gene expression in adipocytes from lean children: association to metabolic disorders

Project description:Bisphenol A (BPA) is a xenobiotic endocrine disrupting chemical. In vitro and in vivo studies indicated that BPA alters endocrine-metabolic pathways in adipose tissue increasing the risk of developing metabolic disorders. BPA effects on human adipocytes, specifically in children, are poorly investigated. To investigate in childhood the effect of exposure to BPA on metabolic disorders we analyzed in vitro the effects of environmentally relevant doses of BPA on gene expression of mature human adipocytes from pre-pubertal lean patients and on related physiological outcomes. Adipocytes from children were treated in vitro with BPA and gene expression was evaluated by qRT-PCR. Genome wide analyses were performed using GeneChip® Human Gene 1.0 ST array. Lipid content in adipocytes was estimated by ORO staining and Triglyceride Quantification Kit. Secreted IL-1β, in adipocytes culture medium, and insulin, in PANC-1 culture medium, were performed using ELISA assays. BPA was found to promote up-regulation of ERα and ERRγ, and down-regulation of GPR30 expression modulating estrogen signaling and following a non-linear dose-response. Microarray data analysis demonstrated that BPA increases the gene expression of pro-inflammatory cytokines and lipid metabolism-related FABP4 and CD36 in adipocytes. PCSK1 resulted the most interesting gene being down-regulated by BPA thus impairing insulin production in pancreas. BPA promotes inflammation and lipid metabolism dysregulation in adipocytes from lean children. Moreover, PCSK1 can be a key gene in BPA action modulating insulin production. Exposure to BPA in childhood may be an important risk factor in developing obesity and metabolic disorders.

2015-07-09 | GSE58516 | GEO

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