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This Article Full Text Full Text (PDF) All Versions of this Article: 69/1/195    most recent biolreprod.102.013870v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tsuboi, K. Articles by Ichikawa, A. Search for Related Content PubMed PubMed Citation Articles by Tsuboi, K. Articles by Ichikawa, A. Agricola Articles by Tsuboi, K. Articles by Ichikawa, A.

Role of Prostaglandin H₂ Synthase 2 in Murine Parturition: Study on Ovariectomy-Induced Parturition in Prostaglandin F Receptor-Deficient Mice¹

Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606–8501, Japan

To determine the prostaglandin (PG) H₂ synthase (generally referred to as cyclooxygenase [COX]) isozyme responsible for producing uterotonic PGs during parturition, we used PGF₂ receptor-deficient mice, which exhibit parturition failure due to impaired withdrawal of serum progesterone at term. On ovariectomy-induced parturition in these mice, uterine COX-2 mRNA expression was drastically induced in the myometrium, whereas COX-1 mRNA expression in the endometrial epithelium decreased. The concomitant administration of progesterone with ovariectomy resulted in a delay in parturition and the disappearance of both the increase in COX-2 mRNA and the decrease in COX-1 mRNA. Thus, the expression of myometrial COX-2 and the occurrence of parturition are closely associated in this model. Furthermore, administration of the COX-nonselective inhibitor, indomethacin, or the COX-2-selective inhibitor, Dup-697 or JTE-522, effectively delayed ovariectomy-induced parturition in these mice. These findings suggest that COX-2-derived PGs contribute to the onset of parturition after the decrease in serum progesterone level.

¹ This work was supported in part by the grants from the Mochida Memorial Foundation for Medical and Pharmaceutical Research; the Sankyo Foundation of Life Science, the Takeda Science Foundation, and Grants-in-aid for Scientific Research from the Ministry of Education, Culture, Sports Science and Technology of Japan.

² Correspondence: Atsushi Ichikawa, Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606–8501, Japan. FAX: 81 75 753 4557; aichikaw{at}pharm.kyoto-u.ac.jp

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