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Formyl-Methionyl-Leucyl-Phenylalanine Induces Prostaglandin E₂ Release from Human Amnion-Derived WISH Cells by Phospholipase C-Mediated [Ca²⁺]_i Rise¹

^a Department of Biology, ^b Section of General Physiology, University of Ferrara, 44100-I Ferrara, Italy Department of Morphology and Embryology, ^c Section of Human Anatomy, University of Ferrara, 44100-I Ferrara, Italy Department of Biomedical Sciences and Advanced Therapy, Section of Obstetrics and Gynecology, University of Ferrara, 44100-I Ferrara, Italy

ABSTRACT

The presence of binding sites for formyl-methionyl-leucyl-phenylalanine (fMLP), its effect on prostaglandin E (PGE) release, and the signal transduction pathway activated by the peptide were investigated in human amnion-derived WISH cells. Our results demonstrate that specific binding sites for fMLP are present on WISH cells and that the peptide induces a significant increase of prostaglandin (PG)E₂ release. The kinetic properties of binding are similar to those previously found in amnion tissue prior to the onset of labor, i.e., only one population of binding sites with low affinity for the peptide is present. Binding of ³H-fMLP in WISH cells is inhibited by N-t-butoxycarbonyl-methionyl-leucyl-phenylalanine, an fMLP receptor antagonist, with an IC₅₀ value very close to that shown by nonlaboring amnion. The fMLP-induced PGE₂ output is inhibited by indomethacin, quinacrine, and U-73122, inhibitors of cyclooxygenase, phospholipase A₂, and phospholipase C, respectively. As regards the transduction pathway activated by fMLP, we demonstrate that phospholipase C activation, followed by an increase of intracellular calcium concentration ([Ca²⁺]_i), is involved in response to the peptide. Our results add further evidence to the role of proinflammatory agents in the determination of labor. Furthermore, because WISH cells appear to behave like nonlaboring amnion tissue, they represent the ideal candidate for in vitro investigation of the events triggering the mechanism of delivery.

FOOTNOTES

First decision: 6 September 2000.

¹ Supported by grants from Ministero dell'Università e della Ricerca Scientifica e Tecnologica and a grant for biomedical research from Azienda Ospedaliera "Arcispedale Sant'Anna," University of Ferrara.

² Correspondence: Carla Biondi, Department of Biology, Section of General Physiology, University of Ferrara, via L. Borsari, 46, 44100-I Ferrara, Italy. FAX: 0532 207143; clm{at}dns.unife.it

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