CONTROL OF PORCINE GRANULOSA CELL ESTROGEN SECRETION

哺乳动物的卵泡产生和分泌类固醇激素， 调节生殖系统各组成部分的功能。卵巢的命运 卵泡有：1)变性(闭锁)和2)排卵、黄体生成、 黄体形成。研究表明，在猪和其他动物中 卵泡发育的终末步骤是：1)丧失 产生卵泡类固醇产品雌激素(E)的能力 2)获得生产黄体类固醇产品的能力 孕酮(P)。这种现象可称为E-P漂移。这些终端 台阶似乎同时发生在闭锁和排卵/卵巢化过程中。 过渡。本申请中的初步数据显示，有一个组件 的猪卵泡(颗粒细胞)表现出相同的序列 在体外放置时的末端台阶。从E-P的第一步开始 轮班是E生产的损失，有可能是信号造成的 因为这种丧失会导致闭锁和排卵/黄体生成。 过渡。在请求的支持期间，该项目将调查 猪颗粒细胞产生E的控制如下：1)形成一种 猪卵泡颗粒细胞特征的完整描述 E-P漂移与E产生损失的体外模型。这个 采用的方法学将确定E底物的代谢物 生产和工艺的相对重要性可能会转移这一点 底物。2)在获得体外E-P漂移的描述后， 将在体外寻找支持相同现象的证据 猪卵巢。所采用的方法将是组织化学检查 卵巢寻找卵泡酶活性从E-P转变的证据 闭锁和排卵前卵泡的产生 黄体化。此外，卵泡窦液中的类固醇激素也会 检查是否有E-P转换的证据。3)将启动研究以 E产能损失的控制机制。五花八门 荷尔蒙机制将使用体外模型进行研究 识别启动E-P转换的信号。中国未来的发展方向 该项目将涉及：1)进一步努力确定哪些信号 造成E生产能力损失，以及2)具体研究 调节这一信号作用的细胞内机制。通过 开发和研究E-P转换的体外模型，本项目 将提供对闭锁和闭锁机制的洞察 排卵/黄体化过渡。

Mammalian ovarian follicles produce and secrete steroid hormones which regulate the function of reproductive system components. Fates of ovarian follicles are: 1) degeneration (atresia) and 2) ovulation, luteinization, and corpus luteum formation. Studies have shown in the pig and other species that the terminal steps in follicular development are: 1) loss of ability to produce the follicular steroid product estrogen (E) followed by 2) acquisition of capability to produce the luteal steroid product progesterone (P). This phenomenon can be termed E-P shift. These terminal steps appear to occur both in atresia and in the ovulation/uteinization transition. Preliminary data in this application show that one component of the pig follicile (granulosa cells) exhibit the same sequence of terminal steps when placed in vitro. Since the initial step in the E-P shift is loss of E production, it is possible that the signal responsible for this loss induces both atresia and the ovulation/luteinization transition. In the requested support period, this project will investigate control of E production by pig granulosa cells as follows: 1) Develop a complete description of characteristics of the porcine granulosa cell in vitro model for the E-P shift with regard to loss of E production. The methodology employed will identify metabolites of the substrate for E production and the relative importance of process with may divert this substrate. 2) After obtaining the description of the E-P shift in vitro, evidence will be sought which supports the same phenomenon in vitro in the pig ovary. The methodology employed will be histochemical examination of ovaries for evidence of a shift in follicular enzyme activity from E-P production in folliciles undergoing atresia and preovulatory luteinization. In addition, follicular antral fluid steroids will be examined for evidence of the E-P shift. 3) Studies will be initiated into the mechanism which controls the loss of E production capability. Various hormonal mechanisms will be investigated using the in vitro model to identify the signal which initiates the E-P shift. The future course of the project will involve: 1) further efforts to identify the signal which causes loss of E production capability, and 2) study of the specific intracellular mechanisms which mediate actions of this signal. By developing and studying a in vitro model for the E-P shift, this project will provide insight into the mechanisms of atresia and ovulation/luteinization transition.