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Stimulation of Human Trophoblast Invasion by Placental Growth Hormone

Institut National de la Santé et de la Recherche Médicale (INSERM), Unité 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, Unité 584 (V.G.) Faculté de Médecine Necker, 75730 Paris, France; INSERM, Unité 468 (J.P.) Hôpital Henri Mondor, 94010 Créteil, France; and Laboratoire d’Endocrinologie (A.I.), Université de Liege, B-420 Liege, Belgium

Address all correspondence and requests for reprints to: M. C. Lacroix, Institut National de la Recherche Agronomique, Neurobiologie de l’Olfaction et de la Prise Alimentaire, Domaine de Vilvert, 78352 Jouy en Josas cedex, France. 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 GH/prolactin family are expressed at the maternofetal interface. Because they are involved in cell motility in various models, we examined the possible regulatory role of human placental GH (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 human GH receptor (hGHR). These data were confirmed by in situ immunohistochemistry. EVCT expressed the full-length and truncated forms of hGHR, and the Janus kinase-2/signal transducer and activator of transcription factor-5 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. hPGH stimulated EVCT invasiveness, and this effect was inhibited by a Janus kinase-2 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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