Progestin-Epidermal Growth Factor Regulation of Tissue Factor Expression during Decidualization of Human Endometrial Stromal Cells1

Charles J. Lockwood, Graciela Krikun, R RUNIC, Lisa Barrie Schwartz, Augusto F. Mesia, Frederick Schatz
In: The Journal of Clinical Endocrinology & Metabolism · 2000 · vol. 85(1) , pp. 297–301 · doi:10.1210/jcem.85.1.6292 · PMID:10634402 · W2022260285
article OA: bronze CC0 ⤵ 4 in-corpus citations
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Progestin-induced decidualization of human endometrial stromal cells elevates tissue factor expression via epidermal growth factor receptor activation, mediated by increased receptor levels.

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Abstract

Perivascular decidualized human endometrial stromal cells (HESCs) are ideally positioned to prevent peri-implantational hemorrhage during endovascular trophoblast invasion by expressing tissue factor (TF), the primary cellular mediator of hemostasis. Earlier in vivo and in vitro studies have demonstrated enhanced TF expression in estradiol (E2)-primed HESCs during progestin-induced decidualization. However, the absence of estrogen or progesterone response elements from the TF gene promoter suggests that paracrine factor(s) may mediate these effects. We now demonstrate that significant elevation of TF messenger RNA and protein levels in the cultured HESCs require incubation with both epidermal growth factor (EGF) and the progestin medroxyprogesterone acetate (MPA) added, with or without E2. By contrast, no effects were elicited by adding EGF with E2, or by the separate additions of EGF, MPA, or E2 plus MPA. Our finding, that transforming growth factor-alpha, but not transforming growth factor-beta or interleukin 1-beta mimics these EGF effects, indicates that progestin-enhanced TF expression in cultured HESCs requires activation of the EGF receptor (EGFR). Western blot analysis indicated that MPA increased EGFR levels 2-to 3-fold in cultured HESCs. The current results suggest that the progestin up-regulation of TF levels in decidualized HESCs is mediated by enhanced EGFR expression.

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