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TGF-β signaling links early-life endocrine-disrupting chemicals exposure to suppression of nucleotide excision repair in rat myometrial stem cells

ABSTRACT: Environmental exposure to endocrine-disrupting chemicals (EDCs) is associated with uterine fibroids (UFs) development, the most common benign tumors in women of reproductive age. It has been shown that UFs originate from abnormal myometrial stem cells (MMSCs) and there is evidence that defective DNA repair capacity could be involved in the emergence of mutations with implications for tumorigenesis. Moreover, the multifunctional cytokine TGF-β1 has been related to UF progress and some works revealed its connection with certain DNA damage repair pathways. Eker rats develop spontaneous uterine tumors in adulthood, which makes it a useful model for the study of UFs emergence The purpose of this study was to evaluate the impact of endocrine-disrupting chemicals (EDCs exposure on TGF-β1 pathway and nucleotide excision repair (NER) capacity, on Eker rat myometrial stem cells (MMSCs).

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE225636 | GEO | 2023/08/07

REPOSITORIES: GEO

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Developmental Reprogramming of Myometrial Stem Cells by Endocrine Disruptor Linking to Risk of Uterine Fibroids [RRBS]

Project description:We report that developmental exposure to the endocrine disrupting chemical (EDC) diethylstilbestrol increases the estrogen action in myometrial stem cells (MMSCs), the origin from which UFs originate. The expression of reprogrammed estrogen responsive genes (ERGs) is driven by activated mixed lineage leukemia protein-1 (MLL1) in MMSCs. Deactivation of MLL1 reverses reprogramming of ERG expression. In addition, upregulation of ERGs occurs via DNA hypomethylation mechanism. Furthermore, the secretome of reprogrammed MMSCs enhances the proliferation of differentiated myometrial cells through activation of β-catenin signaling. This work identifies epigenetic mechanisms of MLL1/DNA methyltransferase- mediated MMSC reprogramming, and EDC exposure epigenetically targets MMSCs and imparts a hormonal imprint on the ERGs resulting in a “hyper-estrogenized” phenotype and increased hormone-dependent risk of UFs.

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Developmental Reprogramming of Myometrial Stem Cells by Endocrine Disruptor Linking to Risk of Uterine Fibroids [RNA-Seq]

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Developmental Reprogramming of Myometrial Stem Cells by Endocrine Disruptor Linking to Risk of Uterine Fibroids [ChIP-Seq]

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EDCs gene expression profile in MCF7 cells

Project description:Endocrine disrupting chemicals (EDCs) are compounds that disrupt normal hormonal signaling. Examples are Xenoestrogens (e.g BPA) and Phytoestrogens (e.g isoflavones).

2013-12-31 | GSE45721 | GEO

EDCs gene expression profile in MCF7 cells

Project description:Endocrine disrupting chemicals (EDCs) are compounds that disrupt normal hormonal signaling. Examples are Xenoestrogens (e.g BPA) and Phytoestrogens (e.g isoflavones). Comparison of EDC treated versus vehicle treated MCF7 parental cells. Each comparison in technical and biological duplicate.

2013-12-31 | E-GEOD-45721 | biostudies-arrayexpress

Developmental Exposure to Endocrine-Disrupting Chemicals Alters Gene Expression in Myometrium of Exposed Animals

Project description:The goal of this study was to compare NGS-derived murine myometrial progenitor cell transcriptome profiling (RNA-seq) of an animal model of uterine fibroid tumorigenesis in rats exposed during uterine development to an endocrine-disrupting chemical, diethylstilbestrol (DES) versus vehicle (VEH) control, unexposed animals, to determine the pathways and biological processes, whose gene expression may be altered as a result of the exposure.

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Effects of long-term endocrine disrupting compound exposure on Macaca mulatta embryonic stem cells

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Effects of single or 35 days oral exposure of adult Sprague-Dawley rats to p-tert-octylphenol on uterine gene expression

Project description:Contamination of the environment with endocrine disrupting chemicals (EDCs) has raised concerns about potential health hazards for humans and wildlife. P-tert-octylphenol (OP) is one such ubiquitous chemical reported to bind to the estrogen receptor (ER) and alter expression of estrogen-responsive genes. Human and wildlife exposure to OP are likely, due to its persistence in the environment and its presence in food, water and items of daily use. Detrimental effects of OP exposures on the reproductive system have been observed in some, but not all, in vivo experiments. This study compared estrogenic effects of OP in vitro with those in vivo in adult female rats, attempting to better mimic real-life exposures in adults. In vitro, OP bound to human ER weakly and accelerated proliferation of MCF-7 cells. Adult Sprague-Dawley rats were given OP by gavage either once or daily for 35 days (125 mg/kg body weight). Body and organ weights and ovarian follicle populations were unaltered in OP-exposed adult rats after either time point, despite detectable levels of OP in reproductive organs. Toxicity of OP was demonstrated by a slightly reduced growth rate and slightly altered estrous cycle, but there were no significant estrogen-like changes in histomorphology or microarray analyses of gene expression of uterine tissue. Prepubertal rats exposed by gavage to 125 or 250 mg/kg OP for three days failed to show any uterotrophic effects, although E2 caused a 3-fold increase in uterine weight. Results do not support a dose-dependent, estrogenic mode of action for OP. This SuperSeries is composed of the following subset Series: GSE14527: Effects of single oral exposure of adult Sprague-Dawley rats to p-tert-octylphenol on uterine gene expression GSE14528: Effects of 35 days oral exposure of adult female Sprague-Dawley rats to p-tert-octylphenol on uterine gene expression Refer to individual Series

2009-02-20 | E-GEOD-14530 | biostudies-arrayexpress

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