GENE EXPRESSION IN THE PRIMATE OVULATORY FOLLICLE

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 在哺乳动物物种中，由脑垂体分泌的促性腺激素（尤其是促黄体激素，LH）的中期激增在卵巢中引发级联事件，导致成熟卵泡排卵（即，卵泡壁破裂并释放其封闭的卵母细胞），作为该过程的一部分，促性腺激素激增作用于排卵前卵泡以引起卵丘-卵母细胞成熟，包括卵母细胞中减数分裂的重新启动和周围卵丘细胞的扩增，从而产生可在排卵时从卵泡释放的可受精卵。啮齿动物研究表明，前列腺素（PG）的合成和局部PGE 2受体（通过PGER 2而不是R1）的作用对排卵期事件（包括卵丘-卵母细胞扩增（C-OE））和生育力至关重要。在Stouffer实验室进行的研究表明，恒河猴排卵期卵泡中参与PGE合成的酶以及PGER 2的mRNA水平显著增加。因此，设计了进一步的研究以评价与媒介物对照相比，PGE 2拮抗剂是否：（1）在恒河猴中改变自然月经周期期间的适时排卵，和（2）阻断排卵期卵泡中的C-OE。体内和体外研究表明，PGE 2受体信号促进灵长类动物的C-OE，并提供了一个新的项目，以确定是否PGE 2拮抗剂是一种有效的，可逆的避孕成年，骑自行车的猴子的基本原理。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. 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 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 (C-OE), 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 during the natural menstrual cycle, and (2) blocked C-OE in the periovulatory follicle, in rhesus monkeys. In-vivo and in vitro studies suggest that PGE2-receptor signaling promotes C-OE in primates, and provided the rationale for a new project to determine if a PGE2 antagonist was an effective, reversible contraceptive in adult, cycling monkeys.