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Submitted on November 30, 2004
Accepted on February 8, 2005
INSERM, U-427 (M.C.L., T.F, J.G., V.T., D.E.-B.) and Laboratoire de Génétique Moléculaire (I.L.), Faculté des Sciences Pharmaceutiques et Biologiques, Université René descartes, 75270 Paris, France; Service d'Hormonologie (J.G), Hôpital Robert Debré, 75019 Paris, France; Maternité Port-Royal (V.T.), Höpital Cochin, Université René Descartes, Paris 5, France; INSERM, U-584 (V.G.) Faculté de Médecine Necker, 75730 Paris, France; INSERM, U-468 (J.P.) Hôpital Henri Mondor, 94010 Créteil, France; Laboratoire d'Endocrinologie (A.I.), Université de Liege, B-420 Liege, Belgium
* To whom correspondence should be addressed. E-mail: mlacroix{at}jouy.inra.fr.
A critical step in establishment of human pregnancy is the invasion of the uterus wall by the extravillous cytotrophoblast (EVCT), a process regulated by multiple autocrine and paracrine factors. Hormones belonging to the growth hormone/prolactin family are expressed at the maternofetal interface. As they are involved in cell motility in various models, we examined the possible regulatory role of placental growth hormone (hPGH) in EVCT invasiveness. By using an in vitro invasion model, we found that EVCT isolated from first-trimester chorionic villi and cultured on matrigel, secreted hPGH and expressed hGHR. These data were confirmed by in situ immunohistochemistry. EVCT expressed the full-length and truncated forms of the GH receptor (hGHR) and the JAK2-Stat5 signaling pathway was activated in EVCT by hPGH treatment. Strong hPGH and hGHR expression was observed when EVCT invaded Matrigel and moved through the pores of the filter on which they were cultured. Human PGH stimulated EVCT invasiveness, and this effect was inhibited by a JAK2 inhibitor. Interestingly, hPGH was more efficient than pituitary GH in stimulating EVCT invasiveness. These results offer the first evidence for a placental role of hPGH, and suggest an autocrine/paracrine role of hPGH in the regulation of trophoblast invasion
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