Change in prostaglandin E synthases (PGESs) in microsomal PGES-1 knockout mice in a preterm delivery model

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 m...

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Published inJournal of endocrinology Vol. 187; no. 3; pp. 339 - 345
Main Authors Kubota, Ken, Kubota, Toshiro, Kamei, Daisuke, Murakami, Makoto, Kudo, Ichiro, Aso, Takeshi, Morita, Ikuo
Format Journal Article
LanguageEnglish
Published Colchester BioScientifica 01.12.2005
Portland Press
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ISSN0022-0795
1479-6805
DOI10.1677/joe.1.06169

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Summary: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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ISSN:0022-0795
1479-6805
DOI:10.1677/joe.1.06169