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Ken Kubota Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Comprehensive Reproductive Medicine, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5–8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan

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Toshiro Kubota Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Comprehensive Reproductive Medicine, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5–8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan

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Daisuke Kamei Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Comprehensive Reproductive Medicine, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5–8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan

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Makoto Murakami Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Comprehensive Reproductive Medicine, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5–8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan

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Ichiro Kudo Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Comprehensive Reproductive Medicine, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5–8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan

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Takeshi Aso Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Comprehensive Reproductive Medicine, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5–8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan

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Ikuo Morita Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Comprehensive Reproductive Medicine, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5–8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan

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Most preterm deliveries are associated with infection and inflammation. Prostaglandin E2 (PGE2) is one of the most important mediators in the processes of inflammation, and is converted from PGH2 by various kinds of PGE synthases (PGESs). Among PGESs, microsomal PGES-1 (mPGES-1) is known to be the most important subtype in the processes of inflammation. To evaluate the role of PGESs in preterm delivery, we used mPGES-1 knockout mice in a lipopolysaccharide (LPS)-induced preterm labor model. Unexpectedly, the duration of labor after LPS treatment was not statistically different between C57BL6 wild-type mice and mPGES-1 knockout mice. In wild-type mice, mPGES-1 mRNA and protein expression increased in the myometrium and fetal membrane after LPS treatment. In contrast, the expression of mPGES-2 or cytosolic PGES was not changed by LPS treatment. On mPGES-1 knockout mice, mPGES-2 increased by LPS treatment in myometrium. The present data indicate that mPGES-1 may be involved in LPS-induced preterm labor, but inhibition of mPGES-1 alone may not prevent preterm delivery, because mPGES-2 might compensate for the role of mPGES-1.

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