170. Preeclamptic decidual stromal cells fail to decidualize during co-culture with placental villous explants

Abstract

Introduction Sustained stromal cell decidualization at the maternal fetal interface is vital to the development of placenta and fetus. Recent reports suggest that defective decidualization of endometrial stromal cells (ESCs) may contribute to the development of preeclampsia (PE). We hypothesize that there may be defective communication between the placenta and stromal cells in PE that contribute to suboptimal decidualization. Our aim is to study the interaction between placenta and decidual cells in an ex vivo co-culture model with respect to decidualization and sFlt1 production. Methods Primary decidual stromal cells (DSCs) were isolated from term placentas of normotensive (n = 4; NT-DSCs) and preeclamptic (n = 3; PE-DSCs) pregnant women. Villous explants (VE) were prepared from NT placenta (n = 3) and stored in liquid nitrogen by the process of vitrification. DSCs were subjected to co-culture with VE for 72 h. Prolactin (PRL) and sFLT1 mRNA expression in VE and DSCs were determined by qRT-PCR. Group means were analyzed by one-way ANOVA. p ⩽ 0.05 is considered significant. Results Co-culturing VE with NT-DSC induced a significant increase in the DSC PRL expression (4.78 ± 1.64-fold against control 1.0, p = 0.005) compared to 1.93 ± 0.40 in PE-DSCs. VE co-cultured with NT-DSCs showed a significant downregulation of DSC sFlt1 expression (0.34 ± 0.10; p = 0.02) but not when co-cultured with PE-DSCs (0.37 ± 0.17, p = 0.07). PRL mRNA levels did not significantly change in VE. However, VE co-cultured with NT-DSCs showed a significant downregulation of sFlt1 mRNA expression. Conclusion VE interaction with NT-DSC induced decidualization and downregulation of sFlt1 in the DSCs as well as sFlt1 expression in the VE. This effect was not observed in co-cultures of VE with PE-DSCs. These findings suggest that in addition to being defective to hormone-induced decidualization, PE-DSCs are defective in their interaction with placenta that is necessary for optimal post-implantation decidualization and downregulation of sFtl1.