Ovarian follicle atresia

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Ovarian follicle atresia is the periodic process in which immature ovarian follicles degenerate and are subsequently re-absorbed during the follicular phase of the menstrual cycle. Typically around 20 follicles mature each month and only a single follicle is ovulated. The rest undergo atresia. That single dominant follicle becomes a corpus luteum following ovulation.[1][2][3][4]

Atresia is a hormonally controlled apoptotic process[5] that depends dominantly on granulosa cell apoptosis.

To date, at least five cell-death ligand-receptor systems have been reported in granulosa cells to play a role in atresia regulation.[6][7][3] They are:

  • tumor necrosis factor alpha (TNF alpha) and receptors
  • Fas ligand and receptors[2]
  • TNF-related apoptosis-inducing ligand (TRAIL; also called APO-2) and receptors
  • APO-3 ligand and receptors
  • PFG-5 ligand and receptors

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.[8]

See also

References

  1. ↑ 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. 
  2. ↑ 2.0 2.1 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. 
  3. ↑ 3.0 3.1 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" (– Scholar search). J. Reprod. Dev. 50 (5): 493–514. doi:10.1262/jrd.50.493. PMID 15514456. 
  4. ↑ Hsueh AJ, Billig H, Tsafriri A (December 1994). "Ovarian follicle atresia: a hormonally controlled apoptotic process". Endocr. Rev. 15 (6): 707–24. PMID 7705278. 
  5. ↑ 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. 
  6. ↑ 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. 
  7. ↑ 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" (– Scholar search). J. Reprod. Dev. 54 (5): 314–20. doi:10.1262/jrd.20051. PMID 18603835. 
  8. ↑ Najati V, Ilkhanipour M, Salehi S, Sadeghi-Hashjin G (January 2008). "Role of nitric oxide on the generation of atretic follicles in the rat ovaries". Pak. J. Biol. Sci. 11 (2): 250–4. doi:10.3923/pjbs.2008.250.254. PMID 18817198. 


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