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¹ Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
² Department of Comprehensive Reproductive Medicine, Tokyo Medical and Dental University, 1-5–45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan
³ Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5–8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan

(Requests for offprints should be addressed to I Morita; Email: morita.cell{at}tmd.ac.jp)

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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