REGULATION OF LUTEAL FUNCTION

黄体功能的调节

• 批准号: 3485023
• 负责人: GEULA GIBORI
• 金额: $ 10.14万
• 依托单位: UNIVERSITY OF ILLINOIS AT CHICAGO
• 依托单位国家: 美国
• 财政年份: 1978
• 资助国家: 美国
• 起止时间: 1978-01-01 至 1993-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3485023
• 关键词: adenylate cyclase; androgens; autoradiography; corpus luteum; cyclic AMP; estradiol; estrogen receptors; gel electrophoresis; hormone regulation /control mechanism; laboratory rat; luteinizing hormone; pregnancy; progesterone; prolactin; radioimmunoassay; radiotracer; secretion; serum; somatomammotropin; steroid hormone biosynthesis; testosterone

The maintenance of corpus luteum vascularization, growth and steroidogenesis in the pregnant rat is a complex process involving pituitary, placental and ovarian hormones. Estradiol, formed in the luteal cell from either endogenous or placental androgen substrates. acts locally to stimulate blood supply, cell hypertrophy and steroidogenesis of the corpus luteum previously exposed to prolactin from either pituitary or placenta. The first aim of this study is to investigate the molecular mechanism by which estradiol affects vascularization and growth of the corpus luteum. We will investigate the possibility that estradiol enhances blood supply to the corpus luteum by increasing the content and mRNA for basic fibroblast growth factor, the luteal angiogenic factor. Whether the requirement for prolactin and estradiol for the optimal growth of the rat corpus luteum reflects interaction of these two hormones on the production and action of insulin-like growth factor-I will be determined. We will examine the possibility that estradiol enhances cholesterol availability for progesterone biosynthesis by increasing the formation of both HMG-CoA reductase, the key enzyme in cholesterol biosynthesis, and Sterol Carrier Protein 2, the molecule responsible for cholesterol transport to the mitochondria. The significance and the role of estrogen induced changes in calcium-calmodulin and calcium- phospholipid-dependent phosphorylation of specific proteins in subcellular fractions will be investigated. Since estradiol biosynthesis by the corpus luteum depends upon placental androgens from mid-pregnancy, we will determine the reason why the placenta does not synthesize androgen early in pregnancy and determine, throughout placental development, the content and mRNA levels of cytochrome P450scc and P45017 alpha, the enzymes responsible for progesterone and androgen biosynthesis. Finally, we will investigate the mechanism by which LH, estradiol and calcium- calmodulin controls placental steroidogenesis in the rat.

维持黄体血管性血管化，生长和 怀孕大鼠中的类固醇发生是一个复杂的过程，涉及 垂体，胎盘和卵巢激素。 雌二醇，形成 来自内源性或胎盘雄激素的黄体细胞 基材。在当地起作用以刺激血液供应，细胞 先前的肥大和类固醇生成先前 暴露于垂体或胎盘的催乳素。 第一个 这项研究的目的是通过研究分子机制 雌二醇影响血管的血管化和生长 黄体。 我们将调查雌二醇的可能性 通过增加 含量和mRNA用于基本成纤维细胞生长因子，黄体 血管生成因子。 是否需要催乳素和 雌二醇可用于大鼠叶黄素的最佳生长反映 这两种激素在生产和作用上的相互作用 将确定胰岛素样生长因子-I。 我们将检查 雌二醇增强胆固醇的可能性 通过增加两者的形成，用于孕激素的生物合成 HMG-COA还原酶，胆固醇生物合成的关键酶和 固醇载体蛋白2，负责胆固醇的分子 运输到线粒体。 意义和作用 雌激素诱导钙 - 钙统和钙的变化 特定蛋白质中磷脂依赖性磷酸化 将研究亚细胞分数。 自雌二醇以来 Luteum的生物合成取决于胎盘雄激素 从中期开始，我们将确定胎盘的原因 在怀孕初期不合成雄激素并确定， 在整个胎盘发育中，内容和mRNA水平 细胞色素P450SCC和P45017α，负责的酶 孕酮和雄激素生物合成。 最后，我们会的 研究LH，雌二醇和钙的机制 钙调蛋白控制大鼠的胎盘类固醇发生。