In Utero BPA Exposure Leads to Epigenetic Alterations
Hugh S. Taylor, M.D.
Yale University School of Medicine
NIEHS Grant R01ES010610
Researchers at the Yale University School of Medicine report that in utero exposure to bisphenol-A (BPA) causes diminished methylation of the estrogen response element of the Hoxa10 gene. This finding suggests that permanent epigenetic alteration of estrogen response element sensitivity to estrogen may be a general mechanism by which endocrine disrupting chemicals exert their actions.
BPA is a known endocrine disrupting chemical. It binds to the estrogen receptor tricking the cells' machinery into thinking they are being signaled by estrogen to act in a prescribed manner. The Hoxa10 gene is a homeobox gene which controls uterine growth and development. A homeobox is a DNA sequence found in genes that are involved in the regulation of patterns of development. They are found in animals and plants.
In this study, pregnant mice were treated with BPA. Hoxa10 and protein expression were increased by 25 percent in the reproductive tracts of mice exposed in utero. DNA methylation of Hoxa10 was significantly reduced in both the promoter and intron regions of the gene after BPA exposure. The decrease in methylation led to an increase in binding of the estrogren receptor alpha to the estrogen response element of the gene.
Citation: Bromer JG, Zhou Y, Taylor MB, Doherty L, Taylor HS. Bisphenol-A exposure in utero leads to epigenetic alterations in the developmental programming of uterine estrogen response. FASEB J. 2010 Jul;24(7):2273-80.
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