Abstract
Bisphenol A (BPA), an environmental endocrine-disrupting organic chemical, has been positively associated with the rate of implantation failure of in vitro fertilization. However, the underlying mechanisms remain unclear. To reveal the impact and the underlying mechanism of BPA on the crosstalk between trophoblast and decidual stromal cells (DSCs), we determined whether BPA was able to affect trophoblast invasion in vitro. We found that BPA significantly inhibited CXCL8 expression in DSCs, which hindered trophoblast invasion, and activated the phosphorylation of ERK in DSCs. U0126, an inhibitor of ERK activation, remarkably rescued trophoblast invasion and the inhibition of CXCL8 expression caused by BPA treatment. Moreover, the nuclear estrogen receptor antagonist ICI 182,780 and transmembrane G protein-coupled receptor GPR30 (membrane estrogen receptor) antagonist G15 significantly blocked the phosphorylation of ERK and reversed the reduction of trophoblast invasion. In brief, BPA activated ERK through nuclear and membrane estrogen receptors and inhibited CXCL8 expression in DSCs, thereby affecting their regulation of trophoblast invasion.