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Follicular atresia : ウィキペディア英語版
Follicular atresia
Follicular atresia is the breakdown of the ovarian follicles, which consist of an oocyte surrounded by granulosa cells and internal and external theca cells. It occurs continually throughout a woman's life, as she is born with millions of follicles but will only ovulate around 400 times in her lifetime.〔(M. J. "Follicle dynamics during ovarian ageing." Molecular and cellular endocrinology 163.1 (2000): 43-48. )〕〔(Elizabeth, and Elizabeth A. Young. "Methodological issues in the study of hormone-behavior relations in humans: Understanding and monitoring the menstrual cycle." Sex differences in the brain. From genes to behavior (2008): 63-78. )〕
==Mechanism==
Follicular atresia is inhibited by follicle-stimulating hormone (FSH), which promotes follicle development.〔(Antti, and Aaron JW Hsueh. "Regulation of ovarian follicle atresia." Annual review of physiology 59.1 (1997): 349-363. )〕 Once the follicle has developed, it secretes estrogen, which in high levels decreases secretions of FSH.〔(J. C., et al. "Selective inhibition of follicle-stimulating hormone secretion by estradiol. Mechanism for modulation of gonadotropin responses to low dose pulses of gonadotropin-releasing hormone." Journal of Clinical Investigation 71.2 (1983): 248. )〕 Granulosa cell apoptosis is considered the underlying mechanism of follicular atresia, and has been associated with five ligand-receptor systems involved in cell death:〔(Noboru, et al. "Regulation mechanism of selective atresia in porcine follicles: regulation of granulosa cell apoptosis during atresia." The Journal of reproduction and development 50.5 (2004): 493. )〕
*Tumor necrosis factor alpha (TNFα) and receptors
*Fas ligand and receptors
*TNF-related apoptosis-inducing ligand (TRAIL or APO-2) and receptors
*APO-3 ligand and receptors
*PFG-5 ligand and receptors
Granulosa cell apoptosis is promoted by tumor necrosis factor-alpha (TNFα), though the mechanism of TNFα is unclear.〔(Ravid, et al. "Induction of apoptosis in granulosa cells by TNFα and its attenuation by glucocorticoids involve modulation of Bcl-2." Biochemical and biophysical research communications 294.1 (2002): 51-59. )〕〔(Hakan, I. T. S. U. K. O. Furuta, and A. J. Hsueh. "Estrogens inhibit and androgens enhance ovarian granulosa cell apoptosis." Endocrinology 133.5 (1993): 2204-2212. )〕
Fas antigen, a cell surface receptor protein that is expressed on granulosa cells, mediates signals that induce apoptosis by binding Fas ligand and therefore plays an important role in follicular atresia. Lack of a functional Fas ligand / Fas receptor system has been linked to abnormal follicle development, and greater numbers of secondary follicles as a result of the inability to induce apoptosis.〔(Kazuhiro, et al. "Involvement of Fas antigen in ovarian follicular atresia and luteolysis." Molecular reproduction and development 47.1 (1997): 11-18. )〕
TNF-related apoptosis-inducing ligand TRAIL activates Caspase 3 (CASP3), which in turn interacts with caspases 6, 7, 8, 9, and 10 to induce apoptosis in granulosa cells.〔(Naoko, et al. "Roles of tumor necrosis factor-related apoptosis-inducing ligand signaling pathway in granulosa cell apoptosis during atresia in pig ovaries." Journal of Reproduction and Development 49.4 (2003): 313-321. )〕

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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