User:Jay9Z/Follicular atresia
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.[1][2]
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Overview
Follicular atresia is the breakdown of the ovarian follicles which are made in the ovaries and serve to produce hormones and oocytes. Oocytes are surrounded by granulosa cells and internal and external theca cells.[3] This process occurs continuously throughout a woman’s life, as they are born with millions of follicles, and about 99% of follicles undergo this breakdown. [3] It has been observed that this mechanism is important in regulating and maintaining a healthy reproductive system.
Mechanism
Atresia is a complex, hormonally controlled apoptotic process that depends dominantly on granulosa cell apoptosis. Follicular atresia is inhibited by follicle-stimulating hormone (FSH), which promotes follicle development. Once the follicle has developed, it secretes estrogen, which in high levels decreases secretions of FSH. Granulosa cell apoptosis is considered the underlying mechanism of follicular atresia, and has been associated with five ligand-receptor systems involved in cell death: [4]
- tumor necrosis factor alpha (TNF alpha) and receptors
- Fas ligand and receptors
- 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 induced by tumor necrosis factor-alpha (TNFα), although the mechanism of how it occurs is unclear.[5]
Fas antigen, a cell surface receptor protein, is expressed on granulosa cells and helps mediate signals that induce apoptosis by binding Fas ligand and therefore plays an important role in follicular atresia.[6] 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.
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.
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.
References
- ^ Najati, Vahid; Ilkhanipour, Minoo; Salehi, Shahpar; Sadeghi-Hashjin, Goudarz (2008). "Role of nitric oxide on the generation of atretic follicles in the rat ovaries". Pakistan journal of biological sciences: PJBS. 11 (2): 250–254. doi:10.3923/pjbs.2008.250.254. ISSN 1028-8880. PMID 18817198.
- ^ Luo, Yuxin; Zhu, Yanbin; Basang, Wangdui; Wang, Xin; Li, Chunjin; Zhou, Xu (2021). "Roles of Nitric Oxide in the Regulation of Reproduction: A Review". Frontiers in Endocrinology. 12: 752410. doi:10.3389/fendo.2021.752410. ISSN 1664-2392. PMC 8640491. PMID 34867795.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b Zhou, Jiawei; Peng, Xianwen; Mei, Shuqi (2019). "Autophagy in Ovarian Follicular Development and Atresia". International Journal of Biological Sciences. 15 (4): 726–737. doi:10.7150/ijbs.30369. ISSN 1449-2288. PMC 6429023. PMID 30906205.
- ^ Zhou, Jiawei; Peng, Xianwen; Mei, Shuqi (2019-01-29). "Autophagy in Ovarian Follicular Development and Atresia". International Journal of Biological Sciences. 15 (4): 726–737. doi:10.7150/ijbs.30369. ISSN 1449-2288. PMC 6429023. PMID 30906205.
- ^ Yamamoto, Yuri; Kuwahara, Akira; Taniguchi, Yuka (2015). "Tumor necrosis factor alpha inhibits ovulation and induces granulosa cell death in rat ovaries". Reproductive Medicine and Biology. 14 (3): 107–115. doi:10.1007/s12522-014-0201-5. PMC 4490172. PMID 26161038.
{{cite journal}}: CS1 maint: PMC format (link) - ^ Yang, Runjun; Xu, Shangzhong; Zhao, Zhihui; Li, Junya (2012). "Fas ligand expression and mediated activation of an apoptosis program in bovine follicular granulosa cells". Gene. 493 (1): 148–154. doi:10.1016/j.gene.2011.11.032.