Gonadotropin and Steroid Hormone Control of Spermatogonial Differentiation

Mitchell, Rod; O’Hara, Laura; Smith, Lee B.

doi:10.1007/978-1-4939-7505-1_7

Cited by 3 publications

(6 citation statements)

References 156 publications

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“…Similarly, testosterone production from Leydig cells reaches its peak at approximately the third month and declines to prepubertal levels at 6–9 months. The absence of androgen receptor (AR) expression in immature Sertoli cells during this period delays further spermatogenesis, while anti-Müllerian hormone (AMH) production remains high [ 53 ]. In the testis, shortly after birth, gonocytes undergo proliferation until 6 months of age and differentiate into A dark spermatogonia, which are considered the “true” spermatogonial stem cells (SSCs).…”

Section: Endocrinological and Testicular Changes During Developmentmentioning

confidence: 99%

“…During prepubertal life until the onset of spermatogenesis at puberty, spermatogonia constitute the only germ cell population. In the first year of life, the prepubertal testis harbors immature proliferative Sertoli cells, with fetal Leydig cells persisting until 6 months post-natally, subsequently being replaced by adult Leydig cell precursors (immature Leydig cells) [ 53 , 54 ].…”

Section: Endocrinological and Testicular Changes During Developmentmentioning

confidence: 99%

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Immune Checkpoint Inhibitors and Male Fertility: Should Fertility Preservation Options Be Considered before Treatment?

Ntemou,

Delgouffe,

Goossens

2024

Cancers

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In recent years, immune checkpoint inhibitors (ICIs) have become a viable option for many cancer patients, including specific subgroups of pediatric patients. Despite their efficiency in treating different types of cancer, ICIs are responsible for a number of immune-related adverse events, including inflammatory toxicities, that can affect several organs. However, our knowledge of the impact of ICIs on the testis and male fertility is limited. It is possible that ICI treatment affects testicular function and spermatogenesis either directly or indirectly (or both). Treatment with ICIs may cause increased inflammation and immune cell infiltration within the seminiferous tubules of the testis, disturbing spermatogenesis or testosterone deficiency (primary hypogonadism). Additionally, the interference of ICIs with the hypothalamic–pituitary–gonadal axis may alter testosterone production, affecting testicular function (secondary hypogonadism) and spermatogenesis. This review provides an overview of the available evidence on the potential association between ICIs and the disruption of spermatogenesis, with special focus on ICIs targeting cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), programmed death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1). Moreover, it highlights the need for further investigations and encourages the discussion of associated risks and fertility-preservation considerations between clinicians and patients.

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Section: Endocrinological and Testicular Changes During Developmentmentioning

confidence: 99%

Section: Endocrinological and Testicular Changes During Developmentmentioning

confidence: 99%

Immune Checkpoint Inhibitors and Male Fertility: Should Fertility Preservation Options Be Considered before Treatment?

Ntemou,

Delgouffe,

Goossens

2024

Cancers

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“…The prepubertal testis differs from the adult testis as it goes through a number of cellular modifications driven by changes of the endocrine environment from birth through puberty [18] (Figure 1). Just after birth the gonocytes continue to proliferate till 6 months of age and then they differentiate into A dark spermatogonia which are proposed to be the “true” SSCs [19,20]. Spermatogonia/SSCs is the only germ cell population present during prepubertal life until the onset of spermatogenesis at puberty.…”

Section: Testicular Development and Functionmentioning

confidence: 99%

“…In particular, follicle stimulating hormone (FSH) and luteinizing hormone (LH) release reaches a peak at 4–10 weeks post-natal, before falling to the lowest levels at around 6 months. Similarly, T production from Leydig cells reaches the highest levels at around the third month before dropping to prepubertal levels at 6–9 months [20] (Figure 2). The absence of androgen receptor (AR) expression in immature Sertoli cells does not allow spermatogenesis to progress further during that period, while the production of anti-Müllerian hormone (AMH) remains high.…”

Section: Testicular Development and Functionmentioning

confidence: 99%

“…Around puberty, the pulsatile secretion of gonadotrophin-releasing hormone (GnRH) stimulates a progressive surge in gonadotrophin release with FSH promoting the proliferation of immature Sertoli cells and LH inducing the maturation of Leydig cells (adult Leydig cells), which start to produce T again [20,21]. The increase of T levels stimulates Sertoli cell maturation, which now express AR and are not able to mitotically divide any further, and inhibits AMH expression [21].…”

Section: Testicular Development and Functionmentioning

confidence: 99%

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Oncofertility: Pharmacological Protection and Immature Testicular Tissue (ITT)-Based Strategies for Prepubertal and Adolescent Male Cancer Patients

Ntemou

Alexandri

Lybaert

et al. 2019

IJMS

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While the incidence of cancer in children and adolescents has significantly increased over the last decades, improvements made in the field of cancer therapy have led to an increased life expectancy for childhood cancer survivors. However, the gonadotoxic effect of the treatments may lead to infertility. Although semen cryopreservation represents the most efficient and safe fertility preservation method for males producing sperm, it is not feasible for prepubertal boys. The development of an effective strategy based on the pharmacological protection of the germ cells and testicular function during gonadotoxic exposure is a non-invasive preventive approach that prepubertal boys could benefit from. However, the progress in this field is slow. Currently, cryopreservation of immature testicular tissue (ITT) containing spermatogonial stem cells is offered to prepubertal boys as an experimental fertility preservation strategy by a number of medical centers. Several in vitro and in vivo fertility restoration approaches based on the use of ITT have been developed so far with autotransplantation of ITT appearing more promising. In this review, we discuss the pharmacological approaches for fertility protection in prepubertal and adolescent boys and the fertility restoration approaches developed on the utilization of ITT.

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Chemotherapy drugs cyclophosphamide, cisplatin and doxorubicin induce germ cell loss in an in vitro model of the prepubertal testis

Smart

Lopes

Rice

et al. 2018

Sci Rep

Self Cite

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Long term survival rates for childhood cancers is steadily increasing, however cancer survivors can experience fertility problems as a consequence of chemotherapy treatment. This is particularly problematic for young boys, for whom no fertility preservation treatment is yet established. Here, we have determined the effects on prepubertal mouse testis of three commonly used chemotherapy drugs; cyclophosphamide (using its active metabolite phosphoramide mustard), cisplatin and doxorubicin, exposing testicular fragments to a clinically relevant range of concentrations in vitro. All three drugs induced a specific and highly significant loss of germ cells, including spermatogonial stem cells. In contrast, there was no significant effect on somatic cells, for either Sertoli or interstitial cells. Time course analysis of cleaved Caspase-3 expression showed a significant increase in apoptosis eight hours prior to a detectable decrease in germ cell numbers following exposure to phosphoramide mustard or cisplatin, although this pattern was not seen following doxorubicin-exposure. Moreover, analysis of DNA damage at 16 h showed increased γH2AX expression in response to all three drugs. Overall, results show that cisplatin, doxorubicin and cyclophosphamide all specifically induce loss of germ cells, including of spermatogonial stem cells, in the prepubertal mouse testis at concentrations relevant to human therapeutic exposures.

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Gonadotropin and Steroid Hormone Control of Spermatogonial Differentiation

Cited by 3 publications

References 156 publications

Immune Checkpoint Inhibitors and Male Fertility: Should Fertility Preservation Options Be Considered before Treatment?

Immune Checkpoint Inhibitors and Male Fertility: Should Fertility Preservation Options Be Considered before Treatment?

Oncofertility: Pharmacological Protection and Immature Testicular Tissue (ITT)-Based Strategies for Prepubertal and Adolescent Male Cancer Patients

Chemotherapy drugs cyclophosphamide, cisplatin and doxorubicin induce germ cell loss in an in vitro model of the prepubertal testis

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