Yong Hannah E J, Murthi Padma, Kalionis Bill, Keogh Rosemary J, Brennecke Shaun P
The University of Melbourne, Department of Obstetrics and Gynaecology and Department of Maternal-Fetal Medicine, Pregnancy Research Centre, The Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville 3052, Victoria, Australia.
The University of Melbourne, Department of Obstetrics and Gynaecology and Department of Maternal-Fetal Medicine, Pregnancy Research Centre, The Royal Women's Hospital, Locked Bag 300, Corner Grattan Street and Flemington Road, Parkville 3052, Victoria, Australia.
Pregnancy Hypertens. 2018 Apr;12:189-193. doi: 10.1016/j.preghy.2017.11.002. Epub 2017 Nov 14.
Decidual stromal cells form the largest proportion of maternal cells at the maternal-fetal interface. Our aim was to investigate the role of the pre-eclampsia associated decidual activin receptor, ACVR2A, in regulating trophoblast functions at this interface. St-T1b and HTR-8/SVneo cell lines were used to model decidual stromal and trophoblast cells respectively. St-T1b conditioned medium inhibited HTR-8/SVneo adhesion, proliferation, migration and invasion; all effects that were attenuated by decidual ACVR2A siRNA transfection. These findings suggest that altered decidual ACVR2A expression perturbs the maternal-fetal crosstalk involved in regulating trophoblast function at the interface, which may affect placentation and lead to pre-eclampsia.
蜕膜基质细胞在母胎界面处构成母体细胞的最大比例。我们的目的是研究子痫前期相关的蜕膜激活素受体ACVR2A在调节该界面处滋养层细胞功能中的作用。分别使用St-T1b和HTR-8/SVneo细胞系模拟蜕膜基质细胞和滋养层细胞。St-T1b条件培养基抑制HTR-8/SVneo细胞的黏附、增殖、迁移和侵袭；而蜕膜ACVR2A siRNA转染可减弱所有这些作用。这些发现表明，蜕膜ACVR2A表达的改变扰乱了参与调节界面处滋养层细胞功能的母胎相互作用，这可能影响胎盘形成并导致子痫前期。
