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(Requests for offprints should be addressed to E Y Adashi who is now at Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Utah Health Sciences Center, 546 Chipeta Way, Mailbox #20, Salt Lake City, Utah 84108, USA)
(S G Derman is now at 3131 Princeton Pike, Bldg. 3, Lawrenceville, New Jersey 08648, USA)
(S Kol is now at Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel)
(I Ben-Shlomo is now at Department of Obstetrics and Gynecology, Haemek Medical Center, Afula, Israel)
Transforming growth factor ß1 (TGFß1) acts as an inhibitor of the actions of interleukin-1ß (IL-1ß) in various organ systems. In order better to understand the interactions between these polypeptides in the ovary, we evaluated the effect of TGFß1 co-treatment on various IL-1ß-mediated actions in cultures of whole ovarian dispersates. Treatment with IL-1ß enhanced media accumulation of nitrites (4.8- fold), prostaglandin E2 (PGE2, 3.9-fold) and lactate (2.0-fold), and enhanced glucose consumption (2.1-fold). Treatment with TGFß1 alone did not significantly affect any of these parameters. However, the addition of TGFß1 inhibited IL-1ß-stimulated nitrite (100%), PGE2 (44%) and lactate (78%) accumulation and inhibited IL-1ß-stimulated glucose consumption (74%) in a dose-dependent manner. The addition of TGFß1 also suppressed the steady-state levels of IL- 1ß-stimulated IL-1ß, type I IL-1 receptor and IL-1 receptor antagonist transcripts (98, 67 and 83% inhibition respectively). These data suggest that TGFß1 is capable of inhibiting several IL- 1ß-stimulated endpoints. Since IL-1 has been identified as a possible proinflammatory mediator of ovulation and TGFß has been implicated as a a promotor of fibrosis and healing, we speculate that IL-1 and TGFß might play antagonistic roles in the normal ovulatory sequence.
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Journal of Endocrinology