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Change in prostaglandin E synthases (PGESs) in microsomal PGES-1 knockout mice in a preterm delivery model
Ken Kubota1, Toshiro Kubota, Daisuke Kamei
1Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
Abstract:
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.
Insights
Microsomal prostaglandin E synthase-1 (mPGES-1) plays a role in infection-induced preterm labor. However, its inhibition alone may not prevent preterm birth due to compensatory mechanisms involving mPGES-2.
Area of Science:
- Reproductive biology
- Inflammation research
- Biochemistry
Background:
- Preterm delivery is often linked to infection and inflammation.
- Prostaglandin E2 (PGE2) is a key mediator of inflammation.
- Microsomal prostaglandin E synthase-1 (mPGES-1) is a critical enzyme in PGE2 synthesis during inflammation.
Purpose of the Study:
- To investigate the role of prostaglandin E synthases (PGESs) in lipopolysaccharide (LPS)-induced preterm labor.
- To evaluate the function of mPGES-1 in a mouse model of preterm labor.
Main Methods:
- Utilized mPGES-1 knockout mice and wild-type C57BL6 mice.
- Administered lipopolysaccharide (LPS) to induce preterm labor.
- Assessed labor duration and measured mPGES-1, mPGES-2, and cytosolic PGES expression in the myometrium and fetal membranes.
Main Results:
- LPS-induced preterm labor duration was similar in both wild-type and mPGES-1 knockout mice.
- LPS treatment increased mPGES-1 mRNA and protein in wild-type mouse myometrium and fetal membranes.
- LPS treatment increased mPGES-2 expression in the myometrium of mPGES-1 knockout mice, but not mPGES-2 or cytosolic PGES in wild-type mice.
Conclusions:
- mPGES-1 is involved in LPS-induced preterm labor.
- Inhibition of mPGES-1 alone may not be sufficient to prevent preterm delivery.
- mPGES-2 may compensate for the loss of mPGES-1 function in preterm labor.
