Death receptor 3 is involved in preeclampsia through regulating placental trophoblast cell physiology by inactivating the PI3K/AKT pathway

Abstract Background Preeclampsia (PE) is a pregnancy related disease that affects about 5% of pregnancies. Death receptor 3 (DR3) expression significantly elevated in both placental tissue and plasma PE patients. However, whether DR3 was involved trophoblasts pathogenesis are not well elucidated. Objective Our research designed to illustrate the biological roles trophoblasts, as explain its relevant mechanisms. Methods HTR‐8/SVneo cells viability, migration, invasion, apoptosis were assessed using MTT, Transwell assay, flow cytometry analysis, respectively. Levels DR3, PI3K, AKT analyzed via reverse transcription‐quantitative polymerase chain reaction assay. Western blot analysis utilized assess p‐PI3K, p‐AKT, protein expression. Results Upregulation obviously inhibited promoted apoptosis, opposed control‐plasmid group. We also found DR3‐plasmid enhanced cleaved‐caspase3 expression, reduced p‐PI3K p‐AKT p‐PI3K/PI3K or p‐AKT/AKT ratio cells. Importantly, IGF‐1, PI3K/AKT signaling pathway agonist, partially reversed effects on cell signal Conclusion through regulating trophoblast physiology pathway, which might be promising therapeutic target for therapy.