[No authors listed]
Prostaglandins (PGs) have long been known to play roles in various processes of female reproduction; however, the molecular mechanisms therein remained unsolved until recently. This review summarizes the recent progress towards understanding the molecular mechanisms underlying PG actions in fertilization and parturition. A series of studies using EP2-deficient mice demonstrated that after ovulation chemokine signalling in the cumulus cells stimulates integrin activation and cumulus extracellular matrix (ECM) assembly through the RhoA/ROCK/actomyosin pathway, although excessive chemokine signalling disturbs sperm penetration. PGE2-EP2 signalling suppresses such a chemokine signalling and stimulates cumulus ECM disassembly, which contributes to successful fertilization. A series of studies using FP-deficient mice revealed that PGF(2α)-FP signalling induces parturition at least by terminating progesterone production; however, some other EP signals are likely to be involved in parturition by inducing myometrial contraction. Therefore, it should be clarified as to which EP and/or FP receptor signals are physiologically essential for myometrial contraction and successful parturition.
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