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Embryology, Anatomy, and Physiology of the Male Reproductive System
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
By the 6th week, germ cells appear in the genital ridges and the epithelium proliferates to form gonocytes.Failure of migration to the gonadal ridge results in gonadal development failure.Epithelial cells of the genital ridge penetrate the mesenchyme, forming primitive sex cords.
Heterologous Pairing and Fertility in Humans
Published in Christopher B. Gillies, Fertility and Chromosome Pairing: Recent Studies in Plants and Animals, 2020
It is important to realize with regard to human fertility that male and female meiosis, while being processes of similar function, i.e., the production of haploid gametes, are of a very different temporal nature. Initially, the germ cells in both male and female arise in or near the yolk sac endoderm, from where they migrate to areas overlying the mesonephros, which develop into the fetal gonads. From this point on, each sex takes its own separate course of maturation. After proliferating for a number of mitotic divisions, the germ cells in the male invade the tubules of the embryonic testis and become resting gonocytes. This state then lasts until puberty, when meiotic activity commences and the gonocytes progressively become type A and B spermatogonia, 1 and 2° spermatocytes, and, finally, spermatids.
Paediatric Urology
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Jemma Hale, Arash K. Taghizadeh
The transition from neonatal gonocyte to adult dark spermatogonia takes place at 3–12 months in humans. Between the first and fourth years of life the spermatogonia differentiate into B-spermatogonia, and then primary spermatocytes. These then remain quiescent until puberty triggers spermatogenesis. The transformation of the neonatal gonocyte into the adult dark spermatogonia appears to be a crucial stage. It seems to be dependent on the environment of these cells being at 33°C. Failure of the testicle to descend into the scrotum keeps the testis at 37°C and so adversely affects this stage. Transformation from neonatal gonocyte to adult dark spermatogonia includes a reduction in the number of these cells probably reflecting apoptosis of abnormal cells. Failure of the testicle to descend by this stage will result in reduced sperm production but also less removal of abnormal cells probably contributing to increased risk of subsequent malignant transformation. Recognition that this stage takes place quite early has resulted in the British Association of Paediatric Urologist recommending in 2011 earlier orchidopexy. Ideally orchidopexy should be performed between 3–6 months; however, 6–12 months is acceptable.
Differentiation of neonate mouse spermatogonial stem cells on three-dimensional agar/polyvinyl alcohol nanofiber scaffold
Published in Systems Biology in Reproductive Medicine, 2020
Marzieh Ziloochi Kashani, Zohreh Bagher, Hamid Reza Asgari, Mohammad Najafi, Morteza Koruji, Fereshteh Mehraein
Since spermatogenesis begins shortly after birth in rodents, the testicular cells of 3–6-day-old mice were used in this research work. During this period, a population of undifferentiated spermatogonial stem cells arises from a subset of gonocytes which are located within the center of seminiferous tubules (Drumond et al. 2011). These undifferentiated cells are called type Asingle spermatogonia and have classically been considered as the SSC population (Ehmcke et al. 2006). Mitotic division of Asingle produces committed progenitor spermatogonia (i.e., Apaired and Aaligned) which, along with Asingle cells, are collectively regarded as undifferentiated A-spermatogonia according to morphological characteristics (Clermont and Bustos-Obregon 1968; Fayomi and Orwig 2018). Further mitotic divisions of undifferentiated A-spermatogonia generate a series of differentiating spermatogonia, including A1, A2, A3, A4, intermediate, and B spermatogonia. Eventually, type B spermatogonia differentiate into primary spermatocytes that will undergo two meiotic divisions to generate round spermatids. Morphological differentiation (spermiogenesis) of these haploid cells leads to the development of mature sperms.
Molecular characteristics of testicular germ cell tumors: pathogenesis and mechanisms of therapy resistance
Published in Expert Review of Anticancer Therapy, 2020
Khaleel I. Al-Obaidy, Michal Chovanec, Liang Cheng
The general multiple-hit hypothesis of malignant transformation at different stages of life is thought to play a major role in the development of TGCTs, where accumulations of several genetic abnormalities are required for tumorigenesis [12]. The initiating events occur during fetal development leading to arrest/abnormal differentiation, giving rise to precursor lesions under the influence of genetic and environmental factors. A latency period then exists until puberty when the sex hormones influence the testicular cells development and maturation leading to additional genetic abnormalities in the abnormally differentiated/maturated cells completing their malignant transformation [12]. The hypothesis that GCNIS originates from primordial germ cells (PGC) is supported by the facts that the GCNIS cells are morphologically similar to fetal gonocytes and express the same embryonic markers as well [13].
Isolation and molecular characterization of spermatogonia from male Sprague-Dawley rats exposed in utero and postnatally to dibutyl phthalate or acrylamide
Published in Toxicology Mechanisms and Methods, 2019
Nathália P. Souza, Lora L. Arnold, Karen L. Pennington, Merielen G. Nascimento e Pontes, Helio A. Miot, João Lauro V. de Camargo, Samuel M. Cohen
The Pou5f1 gene encodes the protein oct 3/4, which is critical in germ cell embryonic development and is involved in cell pluripotency regulation (Ferrara et al. 2006). During normal perinatal maturation, oct 3/4 expression is reduced as germ cells start to differentiate (Ferrara et al. 2006). In humans, OCT 3/4 positive germ cells have been used as an immunohistochemical marker for TGCT since the tumor is composed of germ cells that did not reach differentiation level (Cools 2014). The protein Kitlg binds to the c-kit protein in germ cells activating signaling pathways that control many important cellular processes such as cell growth and proliferation, survival, and migration (Rajpert-De Meyts et al. 2004; Goddard et al. 2007). This gene is highly expressed in fetal gonocytes but progressive cellular differentiation results in loss of expression (Singh et al. 2011). Mki67 expression is correlated with the occurrence of mitoses and it can be present independently of cellular differentiation (Kausch et al. 2003). These genes were used to investigate the pluripotency, proliferation and mitosis potential in the exposed spermatogonia. The apoptosis potential was evaluated by examining Bak1 expression that promotes apoptosis by binding to and antagonizing the apoptosis suppressor activity of Bcl-2 and other anti-apoptotic proteins. Expression of Bak1 in testicular germ cells is repressed by the Kit-Kitlg pathway (Gilbert et al. 2011).