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- W1002020687 abstract "The ovarian follicle assembles to nest and prepare the oocyte for ovulation. Figure 1 shows that some follicular cells even escort the extruded egg to the site of fertilization in the oviduct. By means of its steroid hormone secretion, the follicle also secures the chances of the embryo to launch a successful implantation in the uterus. To this end, the ovarian follicle undergoes two fundamental processes: a dramatic growth in size to create a minimal cellular mass of secretory cells, followed by acquisition of the functional capacities, the most prominent of which is the making of steroid sex hormones (steroidogenesis). The important ovarian sex hormones are progesterone and estradiol. Both hormones support follicular growth and function, as well as prime the cells of the uterine wall for proper future implantation of the embryo. Ovarian androgens are also essential, as both aromatizable estrogen-precursors and modulators of gonadotropin action. But for the initial phases of follicular development, the pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), control most of the follicle’s life span, acting as trophic agents and inducers of steroidogenesis (1). After ovulation, the ruptured follicle transforms into a powerful endocrine gland, the corpus luteum, which secretes progesterone and estrogen serving to maintain a healthy pregnancy. Whereas in humans, the endocrine role of the corpus luteum is assumed by the placenta at the onset of the second trimester, in rodents the corpus luteum is indispensable until the end of the pregnancy (2). Open image in new window Fig 1 Critical checkpoints during ovarian folliculogenesis are revealed by the disrupted gene technology. The process of folliculogenesis is illustrated from top to bottom. (Left) Factors involved in control of follicular development. (Right) Targeted gene disruptions (or mutations) known to arrest folliculogenesis. Gametes: Onset of folliculogenesis requires the arrival of the female germ cells (top) at the fetal gonad site (103,182). This process can be interrupted by disruption of KL/c-kit, Dazla, or atm genes. Lack of KL/c-kit, Dazla, or atm gene products will consequently prevent the formation of the primordial follicle. (A) Primordial follicle: In most mammals, before birth oogonia are transformed into primary oocytes at meiotic prophase, which become surrounded by a layer of flattened granulosa cells (second from top) (103). (B) Primary follicle: The granulosa cells attain a unilamellar cuboidal morphology. To the best of our knowledge, the factor(s) responsible for the morphological transformation of the granulosa cells is not known. (C) Secondary follicle: A series of mitotic divisions of the granulosa cells attaining four layers, and recruitment of theca cells, mark the formation of this preantral secondary follicle. This formation is still gonadotropin independent. Loss of growth factors or growth-factor receptors, such as growth-differentiation factor 9 (GDF-9) or c-kit, respectively, can inhibit further development of this follicle. (D) Tertiary follicle: This follicle is marked by the formation of the antrum and acquisition of meiotic competence of the oocyte. It depends on growth from FSH, LH, and IGF-1. Disruption of the following genes inhibits further development of this follicle: cyclin D2, FSHβ, and α-subunit of the pituitary glycoprotein hormones and IGF-1. (E) Preovulatory Graafian follicle: FSH, LH, and IGF-1 also control the formation of this follicle, whose granulosa cells produce high levels of estrogens and express LH receptors. (F) Periovulatory follicle: In response to LH surge, the granulosa cells initiate a process of luteinization that is inhibitable if a disruption of the NGFI-A transcription factor results in a marked attenuation of the pituitary LH production. At 2–4 h after LH surge, this follicle extinguishes expression of P450arom and P45017α (Fig. 5A), as well as transiently upregulates expression of prostaglandin H synthase-2 (PGHS-2, COX-2), C/EBPβ transcription factor, and progesterone receptor (PR). Gene disruption of the latter three inhibits ovulation, but allows the mucification of the cumulus and resumption of meiosis (GVB). Lack of ovulation is also observed in ER-α-deficient ovaries, where excessive response to LH causes hemorrhagic cyst formation; most females develop ovarian teratomas due to parthenogenetic activation of oocytes prior to ovulation. On ovulation, the extruded oocyte (first polar body is observable) and accompanying cumulus cells enter the oviducal ampulla, where fertilization commences, as illustrated. In the absence of the zona pellucida (disrupted ZP3), the oocyte and/or the embryo are absorbed by the oviduct wall. Corpus luteum (CL); in rodents, the development and maintenance of this secretory gland during pregnancy depends on pituitary prolactin (PRL) and uterine PRL-like substances (158,181), whereas the trophoblast-made human chorionic gonadotropin (hCG) plays this role in humans. Terminal differentiation of the granulosa cells necessitates a complete arrest of proliferation mediated by the cell-cycle inhibitor p27kip1. Luteolysis: degeneration of the corpus luteum is induced by PGF2α. Therefore, loss of PGF-receptor expression in CL cells does not allow the critical downregulation of progesterone production preceding labor. (Inset) The cellular composition of a follicle includes the oocyte, the corona radiata, and the cumulus, granulosa, and theca interna cells. A basement membrane (BM) divides the compartments of the latter two cell types. In the rat, small atretic follicles give rise to the LH-responsive interstitial tissue, which exhibits high androgenesis capacity. GV, germinal vesicle; ZP, zona pellucida." @default.
- W1002020687 created "2016-06-24" @default.
- W1002020687 creator A5061267007 @default.
- W1002020687 date "2000-01-01" @default.
- W1002020687 modified "2023-09-26" @default.
- W1002020687 title "Molecular Events Defining Follicular Developments and Steroidogenesis in the Ovary" @default.
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