Relaxin and Prostaglandin E2 Regulate Interleukin 11 during Human Endometrial Stromal Cell Decidualization

Decidualization of endometrial stromal cells and IL-11 signaling are essential for embryo implantation in the mouse. We investigated the effects of relaxin (RLX) and prostaglandin E2 (PGE2) on IL-11 secretion by human endometrial stromal cells (HESC) and during cAMP or medroxyprogesterone acetate (P...

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Published inThe journal of clinical endocrinology and metabolism Vol. 90; no. 6; pp. 3458 - 3465
Main Authors Dimitriadis, E., Stoikos, C., Baca, M., Fairlie, W. D., McCoubrie, J. E., Salamonsen, L. A.
Format Journal Article
LanguageEnglish
Published Bethesda, MD Endocrine Society 01.06.2005
Subjects
Biological and medical sciences
Endocrinopathies
Fundamental and applied biological sciences. Psychology
Medical sciences
Vertebrates: endocrinology
Human
Arachidonic acid derivatives
Cytokine
Peptide hormone
Interleukin 11
Prostaglandin E2
Relaxin
Ovarian hormone
Decidualization
Regulation(control)
Uterus
Eicosanoid
Female genital system
Stromal cell
Endocrinology
Endometrium
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Summary:Decidualization of endometrial stromal cells and IL-11 signaling are essential for embryo implantation in the mouse. We investigated the effects of relaxin (RLX) and prostaglandin E2 (PGE2) on IL-11 secretion by human endometrial stromal cells (HESC) and during cAMP or medroxyprogesterone acetate (P)-induced decidualization. cAMP-decidualized HESC secreted high levels of IL-11. RLX, cAMP, or PGE2 increased IL-11 mRNA and IL-11 secretion, with maximal response to RLX and cAMP. Addition of the cAMP/protein kinase A inhibitor Rp-adenosine-3,5-cyclic-monophosphorothioate to either RLX- or PGE2-treated cells decreased IL-11 secretion. Indomethacin treatment decreased IL-11 secretion, which was largely restored by cotreatment with PGE2 or RLX. Cotreatment of HESC with RLX, PGE2, or cAMP and estrogen plus P down-regulated IL-11 mRNA and IL-11 secretion at 24 h, before secretion of prolactin (decidualization marker). Addition of W147AIL-11 (IL-11 signaling inhibitor) reduced prolactin secretion stimulated by RLX or PGE2 and estrogen plus P. This is the first demonstration that cAMP-decidualized HESC secrete IL-11 and that IL-11 mRNA and IL-11 secretion are regulated by RLX and PGE2, partly via a cAMP/protein kinase A-dependent pathway. Blocking IL-11 signaling reduced RLX+P- or PGE2+P-induced decidualization, suggesting that RLX and PGE2 act via IL-11. This is important in understanding implantation and regulation of fertility.
ISSN:0021-972X
1945-7197
DOI:10.1210/jc.2004-1014