Julia A. Taylor
Jennifer Sommerfeld-Sager
Donald E. Tillitt
William A. Ricke
Frederick S. vom Saal
Ramji K. Bhandari
2019
<p><span>Fetal/neonatal environmental estrogen exposures alter developmental programing of the prostate gland causing onset of diseases later in life. We have previously shown </span><i>in vitro</i><span> 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 (</span><i>Esr1</i><span>) 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 </span><i>in vivo</i><span> 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 </span><i>in vivo</i><span>. Expression of </span><i>Esr1</i><span> was elevated by bisphenol A or EE2 exposures, which decreased the global expression of DNA methyltransferase 3A (</span><i>Dnmt3a</i><span>), while methylation of </span><i>Esr1</i><span> 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 </span><i>in vivo</i><span>.</span></p>
application/pdf
10.1093/eep/dvz012
en
Oxford Academic
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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