Molecular Human Reproduction, Vol. 8, No. 7, 636-643,
July 2002
© 2002 European Society of Human Reproduction and Embryology
Uterine physiology |
Interleukin 11 advances progesterone-induced decidualization of human endometrial stromal cells
1 Prince Henry's Institute of Medical Research, P.O.Box 3168, Clayton, Victoria 3168 and 2 The Walter and Eliza Hall Institute of Medical Research and Cooperative Research Centre for Cellular Growth Factors, PO Royal Melbourne Hospital, Victoria, Australia
Differentiation of endometrial stromal cells into decidual cells is crucial for embryo implantation and placentation. Interleukin (IL)-11 signalling is essential for adequate decidualization in the mouse uterus. We examined the role of IL-11 during progesterone-induced decidualization of human endometrial stromal cells over a 1012 day period, using prolactin (PRL) production as a decidual marker. These cells produced biologically active IL-11 and expressed IL-11, IL-11R
and PRL mRNA during decidualization. Neutralization of endogenous IL-11 with an anti-human (hu)IL-11 antibody (AB) reduced production of PRL from day 8 and insulin-like growth factor binding protein (IGFBP)-1, another marker of decidualization, from day 10 of culture. Following AB washout, PRL and IGFBP-1 secretion increased. Addition of recombinant (r)huIL-11 (10 or 100 ng/ml) to endometrial stromal cells increased secretion of PRL from day 4 and IGFBP-1 from day 6 compared with progesterone alone. Morphological signs of differentiation accompanied biochemical differentiation in the progesterone-treated cells and were further induced by exogenous rhuIL-11. Our observations demonstrate that human endometrial stromal cells produce biologically active IL-11, which promotes progesterone-induced decidualization. These results suggest that IL-11 has both paracrine and autocrine actions on human endometrial stromal cells and plays an important role in preparing the human endometrium for implantation.
decidualization/endometrial stromal cells/IL-11/IL-11R
/implantation
3 To whom correspondence should be addressed. E-mail: evdokia.dimitriadis{at}med.monash.edu.au
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