Inverse regulation of the interferon-gamma receptor and its signaling in human endometrial stromal cells during decidualization.
Fertil Steril
; 91(5 Suppl): 2131-6, 2009 May.
Article
en En
| MEDLINE
| ID: mdl-18555234
ABSTRACT
OBJECTIVE:
To investigate whether human endometrial stromal cells (ESCs) express the interferon-gamma-receptor (IFN-gamma R) and whether the process of decidualization or human chorionic gonadotropin (hCG) regulate the IFN-gamma R and its signaling pathway.DESIGN:
In vitro experiment.SETTING:
Research 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 17beta-estradiol, progesterone, recombinant hCG, and IFN-gamma as well as an IFN-gamma R-blocking antibody. MAIN OUTCOME MEASURE(S) We analyzed IFN-gamma R and the phosphorylation of signal transducer and activator of transcription 1 (STAT-1) by flow cytometry. We measured IFN-gamma R and interferon response factor 1 (IRF-1) mRNA using semiquantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR). RESULT(S) The IFN-gamma R is up-regulated in human ESCs during decidualization without affecting the phosphorylation of STAT-1. Stimulation of IRF-1 by IFN-gamma is reduced in decidualized ESCs. We found that hCG neither regulates the IFN-gamma R nor its signaling pathway. CONCLUSION(S) These results show an inverse regulation of the IFN-gamma R 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-gamma-mediated signals from immune cells at the implantation site.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Receptores de Interferón
/
Decidua
/
Endometrio
/
Gonadotropina Coriónica
Límite:
Female
/
Humans
Idioma:
En
Revista:
Fertil Steril
Año:
2009
Tipo del documento:
Article
País de afiliación:
Alemania