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Primordial germ cells: Origin, migration and testicular development
Published in Rajender Singh, Molecular Signaling in Spermatogenesis and Male Infertility, 2019
The gonads initially develop from the mesothelial layer of the peritoneum and are a part of the prenatal development of the reproductive system that eventually forms the testes in males and the ovaries in females. Although the testis and ovary arise from a common primordial structure, the genital ridge, they are remarkably analogous to each other, with distinct mechanisms of gene regulation and cellular organization for their development. Here we focus only on the development procedure of the testis. After migration, the germ cells get covered by surrounding somatic cells, which eventually become the testicular cord by the process of testicular differentiation. This process has to be perfectly regulated and synchronized so that this happens only after the germ cell localization to the gonadal ridge but not before that. Few studies have pointed out that the initiation of testicular development is not entirely dependent on the localization of gonocytes, as many germ cell–deficient mouse models have successfully developed normal testis with adequate endocrine function (52–55). The exact mechanism behind the commencement of testicular development is still elusive in nature. However, the process of transformation of a group of cells to a specific organ in a very short span of time is known to involve three major steps: (a) Sertoli cell specification and expansion, (b) testis cord formation and compartmentalization, and (c) formation of seminiferous tubules from testis cords.
Summary and Development of a New Approach to Senescence
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
The tendency for tin to accumulate in the thymus with apparent biosynthesis into one or more compounds appears reasonable in view of the evidence presented. The actual role of tin is unknown. It may be active in immune response to carcinogenesis and tumor growth. Also, it may serve a regulatory function in the development of the reproductive system.
The urinary and reproductive systems and the external genitalia
Published in Frank J. Dye, Human Life Before Birth, 2019
In this chapter, we begin with the development of the urinary system, which provides a foundation for development of the reproductive system. Last, we consider the development of the external genitalia, to which both the urinary and reproductive systems lead.
Associations of the KiSS-1 and GPR54 genetic polymorphism with polycystic ovary syndrome in Yunnan, China
Published in Gynecological Endocrinology, 2022
Ting Zhao, Qiong Zhang, Xiao Xiao, Xinghua Tao, Meixiu Gao, Wenli He, Xiaomei Wu, Tao Yuan
Kisspeptin plays a pivotal role in regulating reproductive hormone secretion [8]. Recently, the effect of kisspeptin on animal reproductive function has become a new research hotspot. Research on G-protein coupled receptor 54 (GPR54) and its ligand kisspeptin system, via animal and human experiments, shows that it is an important switch (gatekeeper) of the reproductive system and a necessary factor in the initiation of puberty and maintenance of reproductive function [9,10]. Therefore, it is a key regulator of the hypothalamic–pituitary–gonadal (HPG) axis. Kisspeptin can directly activate gonadotropin-releasing hormone (GnRH) neurons and participate in the secretion of GnRH, thereby regulating the initiation of reproduction and development of the reproductive system, and maintaining the balance and stability of the hypothalamic–pituitary–ovarian axis [11]. Kisspeptin, an important link between energy metabolism and reproductive endocrine function, is involved in the regulation of the pathological process of PCOS.
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
Androgens are responsible for normal male masculinization and development, i.e. they promote the growth of the AGD and are associated with apoptosis of nipple anlagen in male rats, causing lack of nipple development (Bowman et al. 2003; Christiansen et al. 2010). Blocking in utero testosterone activity may result in a shortened AGD and nipple retention in the male offspring (Hsieh et al. 2012; Li et al. 2015). In epidemiological studies, shorter AGD in males has been frequently associated with clinically relevant outcomes of reproductive health such as cryptorchidism, hypospadias, poor semen quality, infertility, small testes, and low serum testosterone levels in adulthood (Pasterski et al. 2015; Thankamony et al. 2016; Foresta et al. 2018). Reduced AGD values were observed in Sprague-Dawley and Wistar rats exposed in utero to 300 to 900 mg/kg of DBP (Mylchreest et al. 1998; Martino-Andrade et al. 2009; Li et al. 2015; Souza et al. 2019). We examined AGD at PND4 and nipple retention at PND14. DBP-exposed male pups showed reduced AGD compared to control, in addition to increased frequency of nipple retention. No significant alterations were observed in AA exposed pups. The DBP dose administered in our studies was sufficient to interfere with the endocrine system acting as an anti-androgenic substance, probably modifying the testosterone synthesis/secretion during the development of the reproductive system that could lead to testicular impairment in adulthood. However, we did not measure testosterone levels to support this hypothesis.
Disruptions in the reproductive system of female rats after prenatal lipopolysaccharide-induced immunological stress: role of sex steroids
Published in Stress, 2019
V. M. Ignatiuk, M. S. Izvolskaya, V. S. Sharova, S. N. Voronova, L. A. Zakharova
In this study, we aimed to estimate the influence of increased sex steroid concentrations and their antagonists in the prepubertal period on the development of the reproductive system in females. Our results demonstrate that prenatal LPS exposure delayed VO in the offspring. Estradiol antagonist (fulvestrant, 1.5 mg/kg) treatment during the early postnatal period caused further delay, while testosterone antagonist (flutamide, 20 mg/kg per injection) abolished the LPS-induced effect. The onset of estrus occurred 2–3 days after VO in all groups. Prenatal LPS treatment decreased body weight gain and reduced serum sex steroid (estrogen and testosterone) concentrations, and significant changes in ovarian structure were also observed in offspring. Sex steroid antagonist treatment reduced the level of follicular atresia, increased proportions of primordial and antral follicles, and restored body weight and estradiol production.