Follicular atresia

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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.[1][2]

Mechanism[edit]

Follicular atresia is inhibited by follicle-stimulating hormone (FSH), which promotes follicle development.[3] Once the follicle has developed, it secretes estrogen, which in high levels decreases secretions of FSH.[4] Granulosa cell apoptosis is considered the underlying mechanism of follicular atresia, and has been associated with five ligand-receptor systems involved in cell death:[5]

Granulosa cell apoptosis is promoted by tumor necrosis factor-alpha (TNFα), though the mechanism of TNFα is unclear.[6][7]

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.[8]

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.[9]

Related Diseases[edit]

Undergoing follicular atresia is necessary in order for women to maintain a healthy reproductive system. The inability to regulate granulosa cell apoptosis and undergo follicular atresia has been linked to the development of some hormone-related cancers and chemo-resistance.[10]

References[edit]

  1. ^ [Faddy, M. J. "Follicle dynamics during ovarian ageing." Molecular and cellular endocrinology 163.1 (2000): 43-48.]
  2. ^ [Hampson, 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.]
  3. ^ [Kaipia, Antti, and Aaron JW Hsueh. "Regulation of ovarian follicle atresia." Annual review of physiology 59.1 (1997): 349-363.]
  4. ^ [Marshall, 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.]
  5. ^ [Manabe, 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.]
  6. ^ [Sasson, 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.]
  7. ^ [Billig, 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.]
  8. ^ [Sakamaki, Kazuhiro, et al. "Involvement of Fas antigen in ovarian follicular atresia and luteolysis." Molecular reproduction and development 47.1 (1997): 11-18.]
  9. ^ [Inoue, 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.]
  10. ^ [Kim, J. H., et al. "Differential apoptotic activities of wild-type FOXL2 and the adult-type granulosa cell tumor-associated mutant FOXL2 (C134W)." Oncogene 30.14 (2010): 1653-1663.]