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Endocrine Reviews, doi:10.1210/edrv-17-2-156
Endocrine Reviews 17 (2): 156-186
Copyright © 1996 by The Endocrine Society
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Peptide Signaling in Human Placenta and Membranes: Autocrine, Paracrine, and Endocrine Mechanisms*

FELICE PETRAGLIA, PASQUALE FLORIO, CARMINE NAPPI and ANDREA R. GENAZZANI

Department of Gynecology, Obstetric and Pediatric Sciences, Universities of Modena Modena, Pisa, and Napoli, Italy
Department of Pisa Modena, Pisa, and Napoli, Italy
Department of Napoli Modena, Pisa, and Napoli, Italy

Correspondence: Address reprint requests to: Felice Petraglia, M.D., Department of Obstetrics and Gynecology, University of Pisa, via Roma 35, 56100 Pisa, Italy.

Abstract

I. Introduction: During the last 15 years our concepts of the role and functioning of intrauterine tissues during human pregnancy have been changing. While initially considered solely for their role in the exchange of gas and transfer of nutrients and waste, recent studies emphasize the contribution of placenta, decidua, and amnion-chorion to gestational development.

Indeed, starting in the 1970s, evidence that human placenta is able to produce hormones, cytokines, and growth factors greatly expanded our knowledge of the functioning of intrauterine tissues and their putative roles in the physiology of pregnancy. A growing number of studies has provided strong evidence that fetal membranes (amnion, chorion) and maternal decidua are capable of hormone production and metabolism and, when containing hormonal receptors, serve as endocrine organs (Fig. 1). Intrauterine tissues are a source of brain, pituitary, gonadal, and adrenocortical peptide and steroid hormones, chemically identical to and biologically active as their counterparts. Since neuropeptides and peptide hormones act as cytokines and/or growth factors, placenta and intrauterine tissue offer a tool for investigating multiple functions of peptides (Table 1).

Footnotes

* This work has been supported in part by the Italian National Research Council (CNR)-Targeted Project "Prevention and Control Disease Factors"-Subproject "Maternal-Infant Diseases," Contract 95.00887.PF41.




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