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In vivo effects of short-term treatment with Bisphenol A (BPA) on mice pancreatic islets

ABSTRACT: In vivo effects of short-term treatment with Bisphenol A (BPA) on mice pancreatic islets

PROVIDER: PRJNA521497 | ENA |

REPOSITORIES: ENA

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In vivo effects of short-term treatment with Bisphenol A (BPA) on mice pancreatic islets

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

Transcriptome analysis of bisphenol A (BPA) treated Y79 human retinoblastoma cells

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.

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Maternal exposure to bisphenol-A during pregnancy increases pancreatic beta-cell growth during early life in male mice offspring

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

Bisphenol B and bisphenol AF exposure enhances uterine diseases risks in mouse

Project description:Bisphenol A (BPA) analogs, bisphenol B (BPB) and bisphenol AF (BPAF) have been widely detected in the environment and human products with increasing frequency. However, uterine health risks caused by BPBBisphenol A (BPA) analogs, bisphenol B (BPB) and bisphenol AF (BPAF) have been widely detected in the environment and human products with increasing frequency. However, uterine health risks caused by BPB and BPAF exposure need to be further elucidated. The study aimed to explore whether BPB or BPAF exposure will induce adverse outcomes in uterus. We then performed gene expression profiling using data obtained from mouse uterus exposed to BPB and BPAF at 28 days.

2023-05-12 | GSE223464 | GEO

Short-term effects of Elastase inhibition on human islets protein phosphorylation

Project description:To evaluate the short-term effect of elastase inhibition using telaprevir or sivelestat or DMSO on human islets

2024-02-13 | GSE189986 | GEO

Genome-wide analysis of low dose bisphenol-A (BPA) exposure in human prostate cells

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

BPA impacts on HEK 293 cells

Project description:Bisphenol A (BPA) is an environmental endocrine disruptor which has been detected in almost all human bodies. Many studies have implied that BPA exposure is harmful to human health. Previous studies mainly focused on BPA effects on ER-positive cells. Genome-wide impact of BPA on gene regulation in ER-negative cells is unclear. In the present study, we performed RNA-seq to characterize BPA-induced gene regulation on ER-negative HEK 293 cells.

2014-10-10 | E-MTAB-1959 | biostudies-arrayexpress

Bisphenol A alternatives can effectively substitute for estradiol in promoting cell growth through estrogen receptor alpha in human breast cancer cells

Project description:Plasticizers with estrogenic activity, such as bisphenol A (BPA), have been reported to have potential adverse health effects in humans, especially in fetal and infant stages. Due to mounting evidence and public pressure BPA is being phased out by the plastics manufacturing industry and is being replaced by other bisphenol variants in “BPA-free” products. We have compared estrogenic activity of 7 bisphenol analogues (BPA; bisphenol S, BPS; bisphenol F, BPF; bisphenol AP, BPAP; bisphenol AF, BPAF; bisphenol Z, BPZ; bisphenol B, BPB) in human breast cancer cell lines. We used microarrays to detail the alterations in gene expression profiles associated with MCF-7 cell line exposure to bisphenol A analogues

2017-03-03 | GSE85350 | GEO

Genes responsive to bisphenol A in testicular Sertoli cells

2006-04-13 | GSE4650 | GEO

Transcription profiling of mice testicular sertoli cells from transgenic mice harboring a temperature-sensitive simian virus 40 large T-antigen a treated with bisphenol A to investigate the mechanisms by which bisphenol A (BPA) induces cell death

Project description:We performed global scale microarray analysis to identify detailed mechanisms by which bisphenol A (BPA) induce cell death by using an Affymetrix GeneChip system. Testicular Sertoli TTE3 cells used in the present study were derived from transgenic mice harboring a temperature-sensitive simian virus 40 large T-antigen. Cell death accompanying endoplasmic reticulum stress was observed in the cells treated with 0.2 mM BPA. Of the 22,690 probe sets analyzed, approximately 1,300 genes were down- and up-regulated by a factor of 2.0 or greater in the cells treated with BPA. TTE3 cells were treated with BPA for 0, 3, 6, and 12 h. Total RNA samples were prepared from the cells. Gene expression was analyzed by an Affymetrix GeneChip® system with the Mouse Expression Array 430A which was spotted with 22,690 probe sets. Sample preparation for array hybridization was carried out as described in the manufactures instructions.

2007-11-24 | E-GEOD-4650 | biostudies-arrayexpress

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