Estradiol promotes trophoblast viability and invasion by activating SGK1.

摘要: Abstract Background 17β-Estradiol (E2) is a critical regulator of trophoblast function during pregnancy. Serum- and glucocorticoid-inducible kinase (SGK1) has been shown to regulate specific cellular targets downstream E2. However, whether how SGK1 directly mediates the regulatory effects E2 on trophoblasts functions remain unknown. Methods expression in human villous samples serum levels were measured women with early pregnancy loss (EPL) healthy pregnant women. The effect regulation was assessed using luciferase reporter gene assay Chromatin Immunoprecipitation assay. mediation by including cell viability, invasion related signaling molecules such as B leukemia/lymphoma 6, E-cadherin, matrix metalloproteinase 2, α-ENaC, vascular endothelial growth factor, phosphorylation status FOXO1 AKT evaluated HTR8/SVneo cells transfected knockdown plasmid with/without treatment. Results protein decreased patients EPL compared controls. (10 nM) increased promoter activity through estrogen receptor. E2-activated enhanced cells. abrogated above responses Conclusions viability invasion, suggesting that acts key node regulating cross-talk at feto-maternal interface development placenta might be potential therapeutic target for EPL.