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Coordinate Regulation of Prostaglandin Metabolism for Induction of Parturition in Mice

Departments of Pediatrics, Molecular Biology and Pharmacology, and Obstetrics and Gynecology (S.K.W., T.I., G.A.G., L.M.M., S.K.V., J.W., L.J.M.), Washington University School of Medicine, St. Louis, Missouri 63110; Division of Applied Life Sciences (K.W.), University of East Asia, Shimonoseki, Yamaguchi, Japan 751-8503; and Division of Pharmaceutical Sciences (H.-H.T.), College of Pharmacy, University of Kentucky, Lexington, Kentucky 40536

Address all correspondence and requests for reprints to: Louis J. Muglia, M.D., Ph.D., Washington University School of Medicine, 660 Euclid Avenue, Department of Pediatrics, Box 8208, St. Louis, Missouri 63010. E-mail: . muglia_l{at}kids.wustl.edu

Prostaglandins are essential for the initiation of parturition in mice. The peak in uterine prostaglandin F₂ levels occurs at d 19.0 of gestation, just before the onset of labor. Our studies set out to determine the important regulatory step(s) involved in this increase of prostaglandin F₂. We show that cytosolic phospholipase A₂ mRNA, protein, and activity do not significantly vary during mouse gestation. Rather, our studies demonstrate that cyclooxygenase-1 mRNA is abruptly induced at d 15.5 of gestation, but cyclooxygenase-1 protein levels only gradually increase throughout gestation. In contrast, cyclooxygenase-2 protein remains constant during gestation. We find that prostaglandin F synthase protein increases significantly during gestation reaching peak levels between d 15.5 and d 17.5 of gestation. We also find that the level of prostaglandin dehydrogenase, responsible for degradation of prostaglandins, decreases during late gestation. Taken together these results suggest that the regulation of prostaglandin F₂ is a complex process involving the coordinate induction of synthetic enzymes along with a decrease in degradative enzymes involved in prostaglandin metabolism.

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