The uterus: health and disease
Inverse regulation of the interferon-γ receptor and its signaling in human endometrial stromal cells during decidualization

https://doi.org/10.1016/j.fertnstert.2008.04.015Get rights and content
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Objective

To 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.

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 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.

Key Words

Endometrium
decidualization
implantation
IFN-γR
hCG

Cited by (0)

H.F. has nothing to disclose. K.R. has nothing to disclose. S.K. has nothing to disclose. P.L. has nothing to disclose. M.Z. has nothing to disclose.

Herbert Fluhr and Kristina Ramp contributed equally to this paper and should both be considered first author.