Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 417, Issue C, Pages 191-199Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2015.09.028
Keywords
Bisphenol A; DNA methylation; Fkbp5; Hippocampus; HT22 cells; Estrogen receptor beta
Categories
Funding
- Swiss National Science Foundation [PZ00P3_126319]
- Swedish Research Council Formas
- Swiss National Science Foundation (SNF) [PZ00P3_126319] Funding Source: Swiss National Science Foundation (SNF)
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Bisphenol A (BPA), an abundant endocrine disruptor, affects stress-responsiveness and related behaviors in children. In rats, perinatal BPA exposure modifies stress response in pubertal offspring via unknown mechanisms. Here we examined possible epigenetic modifications in the glucocorticoid receptor gene and its regulator Fkbp5 in hypothalamus and hippocampus of exposed offspring. We found increased DNA methylation of Fkbp5 and reduced protein levels in the hippocampus of exposed male rats. Similar effects were obtained in a male hippocampal cell line when exposed to BPA during differentiation. The estrogen receptor (ER) antagonist ICI 182,780 or ER beta knock-down affected Fkbp5 expression and methylation similarly to BPA. Further, BPA's effect on Fkbp5 was abolished upon knock-down of ER beta, suggesting a role for this receptor in mediating BPA's effects on Fkbp5. These data demonstrate that developmental BPA exposure modifies Fkbp5 methylation and expression in male rats, which may be related to its impact on stress responsiveness. (C) 2015 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
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