Conclusion
The activation of Fas/FasL signaling pathway promotes trophoblast apoptosis induced by oxidative stress. This molecular mechanism relates to the inhibition of Notch1 signaling pathway activation, and the up-regulation of E-cadherin, sFlt-1, and VEGF expression.
Methods
The expression levels of FasL, Fas, and E-cadherin in the villous tissues of patients with RSA and those with artificial abortion in normal pregnancy (Normal) were detected by Western blot. CCK-8, flow cytometry, and wound healing were used to detect cell proliferation, apoptosis, and reactive oxygen species (ROS) level, and cell migration ability. Quantitative reverse transcription PCR (RT-qPCR) and Western blot were used to detect the expression of mRNA and protein of Notch1, FasL, Fas, E-cadherin, PKC, Hesl, sFlt-1, VEGF.
Objective
To investigate the expression of Fas/FasL in human villous trophoblast cell HTR8-S/Vneo of patients with recurrent spontaneous abortion (RSA), and to explore the related function and molecular mechanism of Fas/FasL signaling pathway.
Results
Compared with normal group, the protein expression of FasL, Fas, and E-cadherin in villous tissues of RSA group were increased. HTR-8/SVneo cells in the H/R group had decreased proliferation and migration, increased apoptosis, and up-regulated ROS level compared with the Control group. The activation of Fas/FasL signaling pathway promoted HTR-8/SVneo cell injury in H/R group compared with the Fas/FasL+H/R group. Further RT-qPCR and Western blot experiments revealed that the mRNA and protein expression of Notch1, PKC, and Hesl were decreased in H/R group compared with Control group, while the mRNA and protein expression levels of E-cadherin, sFlt-1, and VEGF were significantly increased.