Hormonal regulation of PGE2 and COX-2 production in rabbit uterine cervical fibroblasts. Sato, T., H. Michizu, K. Hashizume, and A. Ito. 1Department of Biochemistry, Tokyo University of Pharmacy and Life Science, Hachioji, Tokyo 192«hyphen»0392; and 2Laboratory of Reproductive Endocrinology, National Institute of Animal Industry, Tsukuba, Ibaraki 305«hyphen»0901Japan
APStracts 7:0049A, 2000.
Prostaglandins (PGs) cause uterine contraction to initiate labor at term. We investigated the effect of progesterone and 17ß-estradiol on the production of PGE2 in rabbit uterine cervical fibroblasts. When the cervical fibroblasts were treated with interleukin-1a (IL- 1a), the level of PGE2 is augmented in a time- and dose-dependent manner. The IL-1a- augmented PGE2 level was almost completely suppressed by progesterone and estradiol- 17ß at the physiological concentration (0.01 µM), whereas a slight decrease in the basal level of PGE2 was observed in the cervical fibroblasts treated with both hormones at a pharmacological concentration (1 µM). In addition, the level of PGE2 augmented by IL- 1a was due to the increase of cyclooxygenase (COX) activity, which was inhibited by progesterone and estradiol-17ß as well as by indomethacin and a specific COX-2 inhibitor, NS-398, but not by the well-known COX-1 inhibitor, aspirin. Furthermore, progesterone and estradiol-17ß suppressed the IL-1a-augmented COX-2 production but not the constitutive production of COX-1 in rabbit uterine cervical fibroblasts. These results suggest that progesterone and estradiol-17ß prevent the initiation of labor by inhibiting PGE2 production after the suppression of COX-2 production during pregnancy in rabbit. 

Received 27 July 2000; accepted in final form 16 October 2000
APS Manuscript Number A754-0.
Article publication pending J Appl Physiol
ISSN 1080-4757 Copyright 2000 The American Physiological Society.
Published in APStracts on 29 January 2001