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Endocrinology Vol. 144, No. 4 1284-1291
Copyright © 2003 by The Endocrine Society

ARTICLE

Prostaglandin (PG) FP and EP1 Receptors Mediate PGF2{alpha} and PGE2 Regulation of Interleukin-1ß Expression in Leydig Cell Progenitors

Laurence Walch, Emanuela Clavarino and Patricia L. Morris

Population Council (L.W., E.C., P.L.M.) and The Rockefeller University (P.L.M.), New York, New York 10021

Address all correspondence and requests for reprints to: Patricia L. Morris, Center for Biomedical Research, Population Council and The Rockefeller University, 1230 York Avenue, New York, New York 10021. E-mail: p-morris{at}popcbr.rockefeller.edu.

Prostaglandins (PG) mediate IL-1ß regulation of several interleukin mRNAs in progenitor Leydig cells. PGE2 and PGF2{alpha} potently reverse indomethacin (INDO; a cyclooxygenase inhibitor) inhibition of IL-1ß autoinduction. IL-1ß increases PGE2 and PGF2{alpha} production. To determine the PG receptors involved in this regulation, this study established by RT-PCR and Western analyses which specific receptors for PGE2 (EP receptors) and PGF2{alpha} (FP receptors) are expressed in progenitors. Pharmacological characterization of receptors involved in PGE2 and PGF2{alpha} regulation of IL-1ß mRNA levels was ascertained using real-time PCR analyses. FP, EP1, EP2, and EP4 receptor mRNAs and proteins, and an EP3 receptor subtype were detected. IL-1ß treatment (24-h) significantly decreased EP1 receptor levels; INDO abrogated this down-regulation. FP, EP2, and EP4 receptor levels increased after IL-1ß and IL-1ß + INDO. A selective FP agonist, cloprostenol (0.1 µM), and PGF2{alpha} (10 µM) had similar effects on IL-1ß mRNA levels in progenitors treated with IL-1ß + INDO. None of the EP2/EP4 agonists [butaprost, misoprostol, or 11-deoxy PGE1 (10 µM)] affected IL-1ß mRNA levels. In contrast, EP1/EP3 agonists (17-phenyl trinor PGE2 and sulprostone) increased IL-1ß mRNAs in a dose-dependent manner. EP1 receptor subtype-selective antagonist, SC-51322, blocked IL-1ß-induced and [IL-1ß + INDO + 17-phenyl trinor PGE2]-induced increases in IL-1ß mRNAs. Taken together, our data demonstrate that FP and EP1 receptors mediate PGF2{alpha} and PGE2 induction of progenitor IL-1ß expression.




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