REGULATION OF LUTEAL FUNCTION

黄体血管化、生长和发育的维持 怀孕大鼠的类固醇合成是一个复杂的过程，涉及 脑下垂体、胎盘和卵巢激素。雌二醇，形成于 来自内源性或胎盘雄激素的黄体细胞 底物。局部作用刺激血液供应，细胞 既往黄体肥大和类固醇生成 暴露于垂体腺或胎盘中的催乳素。第一 本研究的目的是探讨其分子机制。 哪种雌二醇会影响卵巢的血管形成和生长 黄体。我们将调查雌激素是否有可能 通过增加黄体的血液供应来增加黄体的血液供应 碱性成纤维细胞生长因子在黄体中的含量和mRNA 血管生成因子。是否需要催乳素和 雌二醇对大鼠黄体最佳生长的影响 这两种激素相互作用对血管紧张素转换酶的产生和作用 胰岛素样生长因子-I将被测定。我们将研究 雌二醇提高胆固醇利用率的可能性 通过增加孕酮和孕酮的形成促进孕酮的生物合成 HMG-CoA还原酶，胆固醇生物合成的关键酶，以及 固醇载体蛋白2，与胆固醇有关的分子 运输到线粒体。的意义和作用 雌激素诱导的钙调素和钙调素的变化 细胞内特定蛋白的磷脂依赖性磷酸化 亚细胞组分将被调查。自雌二醇以来 黄体的生物合成依赖于胎盘雄激素 从妊娠中期开始，我们将确定胎盘 不会在怀孕早期合成雄激素并决定， 在整个胎盘发育过程中，其含量和mRNA水平 细胞色素P450scc和P45017α，负责 黄体酮和雄激素的生物合成。最后，我们会 探讨促黄体生成素、雌二醇和钙的作用机制。 钙调蛋白控制大鼠胎盘类固醇的生成。

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.