Exposure to Bisphenol A jeopardizes decidualization and consequently triggers preeclampsia by up-regulating CYP1B1.

Preeclampsia (PE) is a pregnancy-related disease that poses a significant threat to the health of both the mother and the fetus. Previous studies have primarily focused on the role of the placenta in PE pathogenesis; however, normal decidualization is crucial for the subsequent development of the placenta and pregnancy. Bisphenol A (BPA) is an environmental endocrine disruptor commonly used in the synthesis of polycarbonate and epoxy resins. Overexposure to BPA can result in severe reproductive issues. To further investigate the effects of BPA exposure on pregnancy, C57BL/6 mice were continuously exposed to either 0 or 100 mg/kg of BPA in this study. As a result, these mice developed symptoms of hypertension and proteinuria, indicative of PE. Additionally, their decidualization process was impaired. Transcriptome sequencing of artificially induced decidua revealed a significant upregulation in the expression of CYP1B1 within the BPA-treated group. This upregulation accelerated the metabolism of estrogen and progesterone, leading to significant decreases in their levels. Furthermore, the expression levels of estrogen and progesterone receptors and their responding genes were significantly reduced. These findings suggest that BPA exposure can negatively impact decidualization and placental development, potentially contributing to the development of PE.