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J Appl Physiol 90: 1227-1231, 2001;
8750-7587/01 $5.00
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Vol. 90, Issue 4, 1227-1231, April 2001

Hormonal regulation of PGE2 and COX-2 production in rabbit uterine cervical fibroblasts

T. Sato1, H. Michizu1, K. Hashizume2, and A. Ito1

1 Department of Biochemistry, Tokyo University of Pharmacy and Life Science, Hachioji, Tokyo 192-0392; and 2 Laboratory of Reproductive Endocrinology, National Institute of Animal Industry, Tsukuba, Ibaraki 305-0901, Japan

Prostaglandins (PGs) cause uterine contraction to initiate labor at term. We investigated the effect of progesterone and 17beta -estradiol on the production of PGE2 in rabbit uterine cervical fibroblasts. When the cervical fibroblasts were treated with interleukin-1alpha (IL-1alpha ), the level of PGE2 was augmented in a time- and dose-dependent manner. The IL-1alpha -augmented PGE2 level was almost completely suppressed by progesterone and 17beta -estradiol 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-1alpha was due to the increase of cyclooxygenase (COX) activity, which was inhibited by progesterone and 17beta -estradiol 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 17beta -estradiol suppressed the IL-1alpha -augmented COX-2 production but not the constitutive production of COX-1 in rabbit uterine cervical fibroblasts. These results suggest that progesterone and 17beta -estradiol prevent the initiation of labor by inhibiting PGE2 production after the suppression of COX-2 production during pregnancy in the rabbit.

pregnancy; uterine contraction; parturition; labor; prostaglandin E2; cyclooxygenase-2


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