Regulation of spermatogenic cell apoptosis by the pro-apoptotic proteins in the testicular tissues of mammalian and avian species

Zakariah, Musa; Molele, Reneilwe A.; Mahdy, Mohamed A. A.; Ibrahim, Mohammed I.A.; McGaw, Lyndy Joy

doi:10.1016/j.anireprosci.2022.107158

Cited by 11 publications

(2 citation statements)

References 65 publications

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“… 1 However, exposure of cells to harmful external stimuli can lead to increased cell death. During spermatogenesis and maturation, cell death induced by mechanisms including apoptosis 2 and autophagy, 3 which are widely present in spermatogenic cells, is important for eliminating abnormal spermatogenic cells and ensuring the accurate transmission of genetic information. Importantly, an abnormal increase in spermatogenic cell death can lower the number and quality of sperm, leading to male infertility.…”

Section: Introductionmentioning

confidence: 99%

Cuproptosis mediates copper-induced testicular spermatogenic cell death

Zhang,

Yu,

et al. 2024

Asian Journal of Andrology

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Cuproptosis, a novel mechanism of programmed cell death, has not been fully explored in the context of spermatogenic cells. This study investigated the potential involvement of cuproptosis in spermatogenic cell death using a mouse model of copper overload. Sixty male Institute of Cancer Research (ICR) mice were randomly divided into four groups that received daily oral gavage with sodium chloride (control) or copper sulfate (CuSO4) at 50 mg kg−1, 100 mg kg−1, or 200 mg kg−1, for 42 consecutive days. Mice subjected to copper overload exhibited a disruption in copper homeostasis. Additionally, significant upregulated expression of key cuproptosis factors was accompanied by a significant rise in the rates of testicular tissue cell apoptosis. Immunohistochemical analysis revealed the presence of ferredoxin 1 (Fdx1) in Sertoli cells, Leydig cells, and spermatogenic cells at various stages of testicular development, and the Fdx1-positive staining area was significantly increased in copper-overloaded mice. Mitochondrial dysfunction and decreased adenosine triphosphate levels were also observed, further implicating mitochondrial damage under cuproptosis. Further analyses revealed pathological lesions and blood−testis barrier destruction in the testicular tissue, accompanied by decreased sperm concentration and motility, in copper-overloaded mice. In summary, our results indicate that copper-overloaded mice exhibit copper homeostasis disorder in the testicular tissue and that cuproptosis participates in spermatogenic cell death. These findings provide novel insights into the pathogenic mechanisms underlying spermatogenic cell death and provide initial experimental evidence for the occurrence of cuproptosis in the testis.

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Section: Introductionmentioning

confidence: 99%

Cuproptosis mediates copper-induced testicular spermatogenic cell death

Zhang,

Yu,

et al. 2024

Asian Journal of Andrology

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“…Apoptosis of spermatogenic and Sertoli cells contributes to controlling the development and function of the testis (Ketola et al 2003). It appears that Bcl-2 proteins take part in the apoptosis regulation in testicular cells (Zakariah et al 2022). Bcl-2 and Bax which regulate apoptosis are proteins present in the adult testis and contribute to the differentiation and maturation of cells in this organ (Beumer et al 2000).…”

Section: Introductionmentioning

confidence: 99%

Spermatogenesis disorder and activation of BCL2/Bax apoptosis pathway in the rat testis after co-exposure to PM2.5 and gaseous pollutants: A ‎possible interaction with GATA4 and GATA6

Noshadirad

Parivar

Zarandi

et al. 2023

Preprint

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The exposure of men to particulate matter and gaseous air pollution can ‎seriously threaten spermatogenesis. However, its specific molecular ‎mechanism is a mystery. This in-vivo rat model study has focused on the effect of coexposure to ambient fine particulate matter (PM2.5) plus gaseous pollutants on the oxidant/antioxidant system in the testis and its role in the changes of sex hormones, spermatogenesis, activation of apoptosis BCL2/BAX signaling pathway and GATA4 and GATA4 protein expression in the testis cells. Twenty-one male Wistar albino rats were ‎randomly divided into three groups including the control group (air with the standard condition) and the GAS (gaseous pollutants alone) and Gas + PM2.5 (PM2.5 plus gaseous pollutants) groups exposed for 3 months (4 days a week, 5 h a day). The results revealed that coexposure to gaseous pollutants and PM2.5 significantly decreased sperm motility, sperm count, and the Johnson score, and increased sperm mortality and sperm DNA fragmentation. Also, in the Gas + PM2.5 group, the levels of testosterone and FSH in serum and the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) in the testis significantly decreased, while the level of malondialdehyde (MDA) increased compared to the control group. The expression of BCL2, GATA4, and GATA6 proteins in the testis significantly decreased in the Gas + PM2.5 group, while Bax protein expression increased compared to the control group. Altogether, coexposure to ambient PM2.5 plus gaseous pollutants could induce oxidative stress in the testis and decrease hormone secretion and apoptosis in sperms via activating BCL2/BAX pathway and possible crosstalk with GATA 4 and GATA 6 proteins.

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Stage-specific expression of Toll-like receptors in the seminiferous epithelium of mouse testis

Doğan,

Sandıkçı,

Karagenç

2024

Histochem Cell Biol

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Genes encoding Toll-like receptors (TLRs) are expressed by germ cells in the mouse testis. Nevertheless, the expression of TLRs by germ cells has only been demonstrated for TLR-3, TLR-9, and TLR-11. Furthermore, the expression of each TLR in relation to the stage of spermatogenesis remains uncertain. We aimed in the present study to examine the expression pattern of all TLRs in germ cells throughout the cycle of seminiferous epithelium in the adult mouse testis. Immunohistochemistry was used to evaluate the expression of TLRs. Results of the present study reveal the expression of TLRs by specific populations of germ cells. Expression of TLRs, except for TLR-7, at endosomal compartments, acrosomes, and/or residual bodies was another interesting and novel finding of the present study. We further demonstrate that the expression of TLR-1, -2, -3, -4, -5, -7, -11, -12, and -13 follows a distinct spatiotemporal pattern throughout the cycle of seminiferous epithelium. While TLR-1, -3, -5, -11, and -12 are expressed in all stages, TLR-4 is expressed only in early and middle stages of spermatogenic cycle. On the other hand, TLR-2, -7, and -13 are expressed only in early stage of spermatogenic cycle. Evidence demonstrating the expression of TLRs in a stage specific manner throughout spermatogenesis strengthen the hypothesis that the expression of various TLRs by germ cells is a developmentally regulated process. However, if TLRs play a role in the regulation of proliferation, growth, maturation, and differentiation of germ cells throughout the cycle of the seminiferous epithelium warrants further investigations.

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Regulation of spermatogenic cell apoptosis by the pro-apoptotic proteins in the testicular tissues of mammalian and avian species

Cited by 11 publications

References 65 publications

Cuproptosis mediates copper-induced testicular spermatogenic cell death

Cuproptosis mediates copper-induced testicular spermatogenic cell death

Spermatogenesis disorder and activation of BCL2/Bax apoptosis pathway in the rat testis after co-exposure to PM2.5 and gaseous pollutants: A ‎possible interaction with GATA4 and GATA6

Stage-specific expression of Toll-like receptors in the seminiferous epithelium of mouse testis

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