This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In mammalian species, the midcycle surge of gonadotropin hormone (notably luteinizing hormone, LH) secreted by the pituitary gland, initiates a cascade of events in the ovary leading to ovulation of the mature follicle (i.e., rupture of the follicle wall and release of its enclosed oocyte), as well as conversion of the follicle wall into a new endocrine gland, the corpus luteum. As part of the process, the gonadotropin surge acts on the preovulatory follicle to elicit cumulus-oocyte maturation, including reinitiation of meiosis in the oocyte and expansion of the surrounding cumulus cells, thereby producing a fertilizable egg that can be released from the follicle at ovulation. Rodent studies suggest that prostaglandin (PG) synthesis and local PGE2-receptor (via PGER2 not R1) action is critical for periovulatory events, including cumulus-oocyte expansion, and fertility. Studies performed in the Stouffer laboratory demonstrated significant increases in mRNA levels for the enzymes involved in PGE synthesis, as well as PGER2, in the periovulatory follicle of rhesus macaques. Therefore, further studies were designed to evaluate whether a PGE2 antagonist, compared to vehicle control: (1) altered timely ovulation and/or the subsequent functional lifespan of the corpus luteum during the natural menstrual cycle, and (2) blocked cumulus-oocyte expansion in the periovulatory follicle, in rhesus monkeys.
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