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  • Title: Cyclooxygenase-2-derived endogenous prostacyclin enhances mouse embryo hatching.
    Author: Huang JC, Wun WS, Goldsby JS, Matijevic-Aleksic N, Wu KK.
    Journal: Hum Reprod; 2004 Dec; 19(12):2900-6. PubMed ID: 15489241.
    Abstract:
    INTRODUCTION: The role of prostaglandins (PGs) in embryo hatching remains controversial. In addition, there is no direct evidence that mouse embryos synthesize PGs. METHODS: The effects of endogenous PG on mouse embryo hatching were evaluated by blocking endogenous PG synthesis with indomethacin. Specific cyclooxygenase (COX) inhibitors were used to identify the role of COX-1- and COX-2-derived PGs. An eicosanoid profile was generated by incubating blastocysts with [3H]arachidonic acid and analysing the metabolites by high performance liquid chromatography. The expression and the localization of COX-1, COX-2 and prostacyclin synthase (PGIS) were examined by western blot analysis and immunohistochemistry. RESULTS: The hatching of embryos cultured in 30 microl of protein-free medium was blocked by indomethacin (P = 0.007) or a selective COX-2 inhibitor (P = 0.004). Adding back iloprost, a prostacyclin analogue, abolished the effects of the COX-2 inhibitor. Prostacyclin was the most abundant PG produced by mouse blastocysts, which expressed COX-1, COX-2 and PGIS. COX-1, COX-2 and PGIS were expressed in 4-cell stage embryos and beyond; they were present in the inner cell mass and the trophectoderm of the blastocysts. CONCLUSION: Mouse embryos express COX-1, COX-2 and PGIS which catalyse the formation of PGI2; COX-2-derived PGI2 plays a critical role in embryo hatching.
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