Prostaglandins Involving in Blastocyst Development through Calcium Mediated Signaling Pathway
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Lipid metabolites involved in cellular regulation as signaling mediators. Prostaglandins (PGs), metabolites of lipid are involved to pregnancy at the time of implantation but the functional roles of PGs on embryo development are still controversy and largely unknown. In previous report, the levels of PGE_2 and PGF_(2α) at embryos of morula stage and blastocyst stage were explored (Cheon et al, 1998). In this study, the previous suggestion was confirmed and the possible downstream mediator of prostaglandin E_2 and prostaglandin F_(2α) on the expansion and hatching of mouse embryo was examined. As expected, developmental rate of the blastocyst to expanded stage was a concentration-response curve that showed the highest expansion rate at 10 μM PGE_2, but at 100 μM PGE_2, the rate was decreased. In contrast to the PGE_2, PGF_(2α) stimulated expansion without toxicity at highest concentration. Cotreatment of PGs with indomethacin overcame the inhibitory effects of indomethacin in expansion. Exogenous PGs also improved the development of expanded embryos to the hatching stage. Besides, PGs receptors’ transcripts detected at blastocyst. PGE_2 was caused of calcium fluctuation in the blastocyst but PGF_(2α) did not. The changes of intracellular calcium concentration were different between indomethacin pretreated embryos and non-treated embryos. Based on these results it is suggested that PGs work as paracrine and/or autocrine factors through calcium and the others which were not identified in this study.
Abstract
Lipid metabolites involved in cellular regulation as signaling mediators. Prostaglandins (PGs), metabolites of lipid are involved to pregnancy at the time of implantation but the functional roles of PGs on embryo development are still controversy and largely unknown. In previous report, the levels of PGE_2 and PGF_(2α) at embryos of morula stage and blastocyst stage were explored (Cheon et al, 1998). In this study, the previous suggestion was confirmed and the possible downstream mediator of prostaglandin E_2 and prostaglandin F_(2α) on the expansion and hatching of mouse embryo was examined. As expected, developmental rate of the blastocyst to expanded stage was a concentration-response curve that showed the highest expansion rate at 10 μM PGE_2, but at 100 μM PGE_2, the rate was decreased. In contrast to the PGE_2, PGF_(2α) stimulated expansion without toxicity at highest concentration. Cotreatment of PGs with indomethacin overcame the inhibitory effects of indomethacin in expansion. Exogenous PGs also improved the development of expanded embryos to the hatching stage. Besides, PGs receptors’ transcripts detected at blastocyst. PGE_2 was caused of calcium fluctuation in the blastocyst but PGF_(2α) did not. The changes of intracellular calcium concentration were different between indomethacin pretreated embryos and non-treated embryos. Based on these results it is suggested that PGs work as paracrine and/or autocrine factors through calcium and the others which were not identified in this study.
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