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Immunopathogenesis and Therapy of Gonadal Disorders and Infertility
Published in George S. Eisenbarth, Immunotherapy of Diabetes and Selected Autoimmune Diseases, 2019
Afollicular premature ovarian failure may result from a variety of causes. Infections have the most impact at periods of high follicle turnover such as at birth, puberty, and peripartum. Viral oophoritis associated with mumps is a common cause.5 Mycobacterial infections, toxins, radiation therapy, chemotherapy (e.g., cyclophosphamide), and surgery exert physical or environmental insult to the ovary.6,7 Congenital disorders may be associated with accelerated follicular atresia. Turner’s syndrome (monosomy X) is associated with a normal number of follicles at 20 weeks gestation and normal histology until the fourth intrauterine month. This is followed by accelerated follicular loss.8-11 Sex chromosome mosaicism 45, XO/46, XX improves ovarian function when compared with Turner’s syndrome, and menstruation may occur in up to 30%.12 Accelerated atresia may also occur in the presence of thymic aplasia.13 An example of this is the athymie nude mouse model. Thymic peptides may stimulate GnRH. Ataxia telangiectasia, myotonia dystrophica, and galactosemia (possible failure of germ cell migration) have all been associated with premature menopause.14 Familial afollicular premature menopause has been reported and may be X-linked dominant or possibly autosomal dominant. Autoimmune disease may also cause an afollicular (or decreased follicular number) form of premature ovarian failure.
Reproductive System and Mammary Gland
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Justin D. Vidal, Charles E. Wood, Karyn Colman, Katharine M. Whitney, Dianne M. Creasy
While follicular atresia is a normal part of ovarian physiology, it may also be seen as a result of xenobiotic treatment through a variety of mechanisms. Atresia of small (primordial or primary) follicles is not commonly observed in adult rodents (Fenwick and Hurst 2002) and is rarely encountered in pharmaceutical development. However, small ovarian follicles have been shown to be susceptible to damage by cytotoxic and mutagenic agents used as chemotherapeutics, heavy metals, industrial chemicals, and irradiation (Generoso et al. 1971; Hooser et al. 1994; Hoyer 2004; Junaid et al. 1997; Nozaki et al. 2009; Plowchalk and Mattison 1992; Sakurada et al. 2009).
Ovotoxic Environmental Chemicals: Indirect Endocrine Disruptors
Published in Rajesh K. Naz, Endocrine Disruptors, 2004
Patrick J. Devine, Patricia B. Hoyer
The ultimate event associated with follicular atresia is the mechanism of physiological cell death, apoptosis.[15] Apoptosis is used by many tissues to delete unwanted cells.[16,17] In distinct contrast to apoptosis, cell death by necrosis is a passive form of cell death that usually occurs in response to injury and elicits an inflammatory response in the surrounding tissue. The ultimate decisive features used to distinguish between apoptosis and necrosis are based upon morphological characteristics.[16] The earliest definitive changes of a cell undergoing apoptosis is compaction of chromatin into dense masses (margination) along the nuclear membrane, condensation of the cytoplasm, and reduction in nuclear size, retained membrane integrity of cytoplasmic organelles. As the process continues, multiple apoptotic bodies (membrane-enclosed structures containing both nuclear and cytoplasmic components) separate from the dying cell, which are quickly phagocytosed by healthy neighboring cells. Contrary to this, necrosis involves organelle and cytoplasmic swelling caused by a destruction of plasma membrane integrity, followed by release of lysosomal enzymes that accelerate membrane disintegration and damage to surrounding cells.
Retinoic acid (all-trans) presents antioxidant properties within human ovary and reduces progesterone production by human granulosa cells
Published in Systems Biology in Reproductive Medicine, 2023
Bruno M. Fonseca, Rebeca Cruz, Beatriz Pinto, Lia Costa, Eduarda Felgueira, Pedro Oliveira, Susana Casal, Irene Rebelo
The retinoids naturally present in mammals exist in different configurations with the atRA the major active form. High FF levels of atRA were positively correlated with patient serum concentrations and with the highest quality embryos (Pauli et al. 2013). It has been shown that human cumulus granulosa cells (CGC) are a primary site of retinoid uptake and atRA biosynthesis supporting the essential role of retinoids in ovarian steroid production and oocyte maturation in mammals (Best et al. 2015). In bovine, atRA may promote cytoplasmic maturation oocytes via its modulatory effects on the gene expression of gonadotrophin receptors, cyclooxygenase-2 and/or nitric oxide synthase in CGC (Ikeda et al. 2005). In addition, follicular atresia is closely related to both apoptosis and autophagy of GC in ovarian follicles (Zhou et al. 2019). The role of atRA and alpha-tocopherol in the human granulosa cells is unclear. Therefore, in a second set of experiments, we adressed the role of atRA and alpha-tocopherol in GC viability and function. Contrary to alpha-tocopherol, GCs exposed to atRA for long periods reduced their viability. It suggests that vitamin A levels disregulation within the human ovary may be detrimental due to its involvement in GC death. Neverthless, we did not observe signals of apoptosis or autophagy of GCs exposed to both atRA and alpha-tocopherol.
The decellularized ovary as a potential scaffold for maturation of preantral ovarian follicles of prepubertal mice
Published in Systems Biology in Reproductive Medicine, 2021
Sanaz Alaee, Raheleh Asadollahpour, Abasalt Hosseinzadeh Colagar, Tahereh Talaei-Khozani
The expression of ECM constituents is regulated by estrogen receptors in mouse ovaries (Zalewski et al. 2012). Constructing a microenvironment similar to that of the in vivo ovarian structure is one of the greatest technical challenges in the fabrication of surrogate ovaries (Pan and Li 2019). Many attempts have been made to mimic the ovarian microenvironment for preserving follicles, preventing follicular atresia, and promoting follicular development (Chiti et al. 2018; Sadr et al. 2018; Cho et al. 2019). Culturing human ovarian slices embedded within 3D polyethylene glycol-fibrinogen hydrogel leads to a decrease in the number of atretic follicles and an increase in granulosa cell proliferation (Lerer-Serfaty et al. 2013). Moreover, embedding the ovarian slices in alginate boosts estrogen secretion and promotes cell division (Lerer-Serfaty et al. 2013; Younis et al. 2017). To reconstruct a surrogate ovary, an appropriate ECM is needed to support folliculogenesis and provide a framework for transplanting the follicle. Artificial ovaries fabricated using decellularized tissues provide natural, biomimicry 3D conditions for follicular development, leading to improved follicle survival (Fisch and Abir 2018). The above indicates the critical role of the ECM in folliculogenesis and in the reconstruction of the ovarian environment for follicular maturation.
The effects of the anti-Müllerian hormone on folliculogenesis in rats: light and electron microscopic evaluation
Published in Ultrastructural Pathology, 2021
It was determined that the number of normal follicles in the further developmental period were decreased in AMH applied experimental groups, especially in 5 µg AMH injected group, compared to the control group. Durlinger et al. reported that AMH inhibits the follicular further development by reducing the sensitivity of granulosa cells to FSH.7 Emily Hayes et al. showed that AMH decreases gene expression that regulates FSH signaling and follicular growth through induction of miRNAs.28 It is reported that primordial follicle recruitment and early primary follicle formation process are gonadotropin independent, and the effects of gonadotropins start from the late primary follicle stage.29 Decreased numbers in secondary follicles that have a normal morphology in AMH applied groups may be owing to the inhibition of primordial follicle recruitment and to the follicular atresia due to the inhibitory effects of AMH to FSH sensitivity of primary follicle granulosa cells, and to interrupted further follicular development. Frequent follicular atresia seen in further follicular stages in the experimental groups supports our views.