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and Progesterone Signaling Pathways in Human Endometrium: Role of PIASy (Protein Inhibitor of Activated Signal Transducer and Activator of Transcription-y)
Institute of Reproductive and Developmental Biology (G.Z., M.C.J., J.M.F., L.F., Y.S.L, M.C., J.J.B), Wolfson & Weston Research Centre for Family Health and Cancer Research-UK Labs and Section of Cancer Cell Biology (S.F.d.M., R.V., E.W.-F.L.), Department of Cancer Medicine, Imperial College London, Faculty of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom
Address all correspondence and requests for reprints to: Dr. Jan Brosens, Institute of Reproductive and Developmental Biology, Wolfson & Weston Research Centre for Family Health, Imperial College London, Faculty of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom. E-mail: j.brosens{at}imperial.ac.uk.
All cardinal events during the reproductive cycle, including ovulation, implantation, and menstruation, are characterized by a profound tissue remodeling and an associated local inflammatory response. The ovarian hormone progesterone is a key modulator of inflammatory signals in reproductive tissues, but the underlying mechanisms are not well understood. In this study, we report that differentiating human endometrial stromal cells (ESCs) acquire resistance to interferon-
(IFN)-dependent signal transducers and activators of transcription (STAT) 1 signaling, although phosphorylation, nuclear translocation, and binding of STAT1 to DNA, are unaffected. These observations prompted an investigation into the role of nuclear repressors of STAT1 signaling. We demonstrate that protein inhibitor of activated STAT-y is complexed to the progesterone receptor (PR) in human ESCs and that its ability to repress STAT1 signaling is dependent upon activation of PR in response to hormone binding. Conversely, IFN and protein inhibitor of activated STAT-y synergistically inhibited PR-dependent transcription, demonstrating that the progesterone and IFN signaling pathways engage in reciprocal transcriptional antagonism in human endometrium.
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