Abstract
Prostaglandin (PG) FP and EP1 receptors mediate PDF2α and PGE2 regulation of interleukin-1β expression in Leydig cell progenitors (HTML)
Walch,Laurence; Clavarino,Emanuela; Morris,Patricia L.
Endocrinology 144(4): 1284-1291
Publication date: 2003
Prostaglandins (PG) mediate IL-1ß regulation of severalinterleukin mRNAs in progenitor Leydig cells. PGE and PGFpotently reverse indomethacin (INDO; a cyclooxygenase inhibitor)inhibition of IL-1ß autoinduction. IL-1ßincreases PGE and PGF production. To determine the PG receptorsinvolved in this regulation, this study established by RT-PCRand Western analyses which specific receptors for PGE (EP receptors)and PGF (FP receptors) are expressed in progenitors. Pharmacologicalcharacterization of receptors involved in PGE and PGF regulationof IL-1ß mRNA levels was ascertained using real-timePCR analyses. FP, EP, EP, and EP receptor mRNAs and proteins,and an EP receptor subtype were detected. IL-1ß treatment(24-h) significantly decreased EP receptor levels; INDO abrogatedthis down-regulation. FP, EP, and EP receptor levels increasedafter IL-1ß and IL-1ß + INDO. A selectiveFP agonist, cloprostenol (0.1 µM), and PGF (10 µM)had similar effects on IL-1ß mRNA levels in progenitorstreated with IL-1ß + INDO. None of the EP/EP agonists[butaprost, misoprostol, or 11-deoxy PGE (10 µM)] affectedIL-1ß mRNA levels. In contrast, EP/EP agonists (17-phenyltrinor PGE and sulprostone) increased IL-1ß mRNAsin a dose-dependent manner. EP receptor subtype-selective antagonist,SC-51322, blocked IL-1ß-induced and [IL-1ß+ INDO + 17-phenyl trinor PGE]-induced increases in IL-1ßmRNAs. Taken together, our data demonstrate that FP and EPreceptors mediate PGF and PGE induction of progenitor IL-1ßexpression.
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