Identification, characterization and biological activity of oxytocin receptor in the developing human penis
by
Vignozzi L, Vannelli GB, Morelli A, Mancina R, Marini M,
Ferruzzi P, Crescioli C, Luconi M, Donati S,
Fisher AD, Baldi E, Filippi S, Forti G, Maggi M.
Department of Clinical Physiopathology,
Andrology and Endocrinology UnitDepartment of Anatomy,
Histology and Forensic Medicine,
Department of Pharmacology and Clinical Physiopathology,
Interdepartmental Laboratory of Functional and Cellular Pharmacology of Reproduction,
University of Florence, 50139 Florence, Italy.
Mol Hum Reprod. 2005 Feb;11(2):99-106


ABSTRACT

Although abnormalities of the male external genitalia (MEG) are a relatively common problem, little is known concerning the molecular mechanisms that finely regulate penile development. We report here the expression of the oxytocin receptor (OTR) gene by real-time RT-PCR in human fetal tissues (11th-12th week of gestation), including the MEG. The developing penis expressed a very high level of OTR mRNA, only a half log(10) unit lower than fetal central nervous system, used as a positive control. The OTR protein is also highly expressed (western, immunohistochemistry and binding studies) and immunolocalized both in the mesenchymal body and in the surrounding blood capillaries, which will later constitute penile trabeculae and sinusoids. Binding studies using [(125)I]oxytocin antagonist ([(125)I]OTA) in cultured human fetal penile smooth muscle cells (hfPSMC) revealed the presence of specific OTR with a high capacity and affinity for oxytocin (OT) and for OTA. Increasing concentrations of OT dose-dependently induced intracellular Ca(2+) mobilization. Furthermore, OTR mediated an increase in the proliferation and the migration of hfPSMC. In conclusion, we demonstrate that in the developing human MEG, OTR is highly expressed and might be involved in coordinating timely and appropriate proliferation and migration of the penile cells. Thus, OTR might represent an additional target for investigating human fetal MEG organogenesis.
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