Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3934455 | Fertility and Sterility | 2009 | 6 Pages |
ObjectiveTo investigate whether human endometrial stromal cells (ESCs) express the interferon-γ-receptor (IFN-γR) and whether the process of decidualization or human chorionic gonadotropin (hCG) regulate the IFN-γR and its signaling pathway.DesignIn vitro experiment.SettingResearch laboratory at a medical university center.Patient(s)Premenopausal women undergoing hysterectomy for benign reasons.Intervention(s)Isolation and incubation of ESCs from hysterectomy specimens with 17β-estradiol, progesterone, recombinant hCG, and IFN-γ as well as an IFN-γR-blocking antibody.Main Outcome Measure(s)We analyzed IFN-γR and the phosphorylation of signal transducer and activator of transcription 1 (STAT-1) by flow cytometry. We measured IFN-γR and interferon response factor 1 (IRF-1) mRNA using semiquantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR).Result(s)The IFN-γR is up-regulated in human ESCs during decidualization without affecting the phosphorylation of STAT-1. Stimulation of IRF-1 by IFN-γ is reduced in decidualized ESCs. We found that hCG neither regulates the IFN-γR nor its signaling pathway.Conclusion(s)These results show an inverse regulation of the IFN-γR and its signaling response via STAT-1 and IRF-1 in human ESCs during decidualization. The early embryonic signal hCG has no effect on this process. This mechanism may finely modulate the reactivity of ESCs to IFN-γ-mediated signals from immune cells at the implantation site.