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.[1][2] Typically around 20 follicles mature each month but only a single follicle is ovulated; the follicle from which the oocyte was released becomes the corpus luteum. The rest undergo follicular atresia.[3][4][5][6]

Mechanism

Atresia is a hormonally controlled apoptotic process[7] that depends dominantly on granulosa cell apoptosis. Follicular atresia is inhibited by follicle-stimulating hormone (FSH), which promotes follicle development.[8] Once the follicle has developed, it secretes estrogen, which in high levels decreases secretions of FSH.[9] Granulosa cell apoptosis is considered the underlying mechanism of follicular atresia, and has been associated with five ligand-receptor systems involved in cell death:[10][11][12][5] They are:

  • tumor necrosis factor alpha (TNF alpha) and receptors
  • Fas ligand and receptors[4]
  • TNF-related apoptosis-inducing ligand (TRAIL; also called 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.[13][14]

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.[15]

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.[16]

In addition, two intracellular inhibitor proteins, cellular FLICE-like inhibitory protein short form (cFLIPS) and long form (cFLIPL), which were strongly expressed in granulosa cells, may act as anti-apoptotic factors.

It has been proposed that enhanced levels of Nitrogen oxide in rats can prevent atresia of the ovarian follicle, and depressed levels have the opposite effect.

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.[17]

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See also

References
  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. Rolaki A, Drakakis P, Millingos S, Loutradis D, Makrigiannakis A (July 2005). "Novel trends in follicular development, atresia and corpus luteum regression: a role for apoptosis". Reprod. Biomed. Online. 11 (1): 93–103. doi:10.1016/S1472-6483(10)61304-1. PMID 16102296.
  4. Manabe N, Matsuda-Minehata F, Goto Y, et al. (July 2008). "Role of cell death ligand and receptor system on regulation of follicular atresia in pig ovaries". Reprod. Domest. Anim. 43. Suppl 2: 268–72. doi:10.1111/j.1439-0531.2008.01172.x. PMID 18638134.
  5. Manabe N, Goto Y, Matsuda-Minehata F, et al. (October 2004). "Regulation mechanism of selective atresia in porcine follicles: regulation of granulosa cell apoptosis during atresia". J. Reprod. Dev. 50 (5): 493–514. doi:10.1262/jrd.50.493. PMID 15514456.
  6. Hsueh AJ, Billig H, Tsafriri A (December 1994). "Ovarian follicle atresia: a hormonally controlled apoptotic process". Endocr. Rev. 15 (6): 707–24. doi:10.1210/edrv-15-6-707. PMID 7705278.
  7. Kaipia A, Hsueh AJ (1997). "Regulation of ovarian follicle atresia". Annu. Rev. Physiol. 59 (1): 349–63. doi:10.1146/annurev.physiol.59.1.349. PMID 9074768.
  8. [Kaipia, Antti, and Aaron JW Hsueh. "Regulation of ovarian follicle atresia." Annual Review of Physiology 59.1 (1997): 349-363.]
  9. Marshall JC, Case GD, Valk TW, Corley KP, Sauder SE, Kelch RP (1983). "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): 248–257. doi:10.1172/JCI110765. PMC 436863. PMID 6401767.
  10. [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.]
  11. Matsuda-Minehata F, Goto Y, Inoue N, Manabe N (October 2005). "Changes in expression of anti-apoptotic protein, cFLIP, in granulosa cells during follicular atresia in porcine ovaries". Mol. Reprod. Dev. 72 (2): 145–51. doi:10.1002/mrd.20349. PMID 16010689.
  12. Matsuda F, Inoue N, Goto Y, et al. (October 2008). "cFLIP regulates death receptor-mediated apoptosis in an ovarian granulosa cell line by inhibiting procaspase-8 cleavage". J. Reprod. Dev. 54 (5): 314–20. doi:10.1262/jrd.20051. PMID 18603835.
  13. [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.]
  14. [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.]
  15. [Sakamaki, Kazuhiro, et al. "Involvement of Fas antigen in ovarian follicular atresia and luteolysis." Molecular reproduction and development 47.1 (1997): 11-18.]
  16. [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.]
  17. [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.]
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