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首页> 外文期刊>Environmental Epigenetics >Estrogen receptor 1 expression and methylation of Esr1 promoter in mouse fetal prostate mesenchymal cells induced by gestational exposure to bisphenol A or ethinylestradiol
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Estrogen receptor 1 expression and methylation of Esr1 promoter in mouse fetal prostate mesenchymal cells induced by gestational exposure to bisphenol A or ethinylestradiol

机译：妊娠暴露于双酚A或炔雌醇诱导的小鼠胎儿前列腺间充质细胞中雌激素受体1的表达和Esr1启动子的甲基化

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摘要

Fetaleonatal environmental estrogen exposures alter developmental programing of the prostate gland causing onset of diseases later in life. We have previously shown in vitro that exposures to 17β-estradiol (E2) and the endocrine disrupting chemical bisphenol A, at concentrations relevant to human exposure, cause an elevation of estrogen receptor α ( Esr1 ) mRNA in primary cultures of fetal mouse prostate mesenchymal cells; a similar result was observed in the fetal rat urogenital sinus. Effects of these chemicals on prostate mesenchyme in vivo are not well understood. Here we show effects in mice of fetal exposure to the estrogenic drug in mixed oral contraceptives, 17α-ethinylestradiol (EE2), at a concentration of EE2 encountered by human embryos/fetuses whose mothers become pregnant while on EE2-containing oral contraceptives, or bisphenol A at a concentration relevant to exposures observed in human fetuses in vivo . Expression of Esr1 was elevated by bisphenol A or EE2 exposures, which decreased the global expression of DNA methyltransferase 3A ( Dnmt3a ), while methylation of Esr1 promoter was significantly increased. These results show that exposures to the environmental estrogen bisphenol A and drug EE2 cause transcriptional and epigenetic alterations to expression of estrogen receptors in developing prostate mesenchyme in vivo .
机译：胎儿/新生儿环境中的雌激素暴露会改变前列腺的发育程序，从而在以后的生活中引发疾病。先前我们已经在体外显示，与人暴露有关的浓度的17β-雌二醇（E2）和内分泌干扰性化学双酚A暴露会导致胎儿小鼠前列腺间充质细胞原代培养物中雌激素受体α（Esr1）mRNA升高。 ;在胎儿大鼠泌尿生殖窦中观察到类似结果。这些化学物质对体内前列腺间充质的作用尚不十分清楚。在这里，我们显示了在混合了口服避孕药17α-炔雌醇（EE2）的胎儿暴露于雌激素药物的小鼠中的浓度，在这种浓度的人胚胎/胎儿的母亲怀孕时，它们在含有EE2的口服避孕药或双酚中受孕。浓度与人体胎儿体内暴露有关。 Esr1的表达通过双酚A或EE2暴露而升高，这降低了DNA甲基转移酶3A（Dnmt3a）的整体表达，而Esr1启动子的甲基化则显着增加。这些结果表明，在体内发展中的前列腺间充质中，暴露于环境雌激素双酚A和药物EE2会引起转录和表观遗传改变雌激素受体的表达。

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