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Sertoli-Leydig Cell Interactions in the Unilaterally Cryptorchid Testis
Published in Tom O. Abney, Brooks A. Keel, The Cryptorchid Testis, 2020
Jeffrey B. Kerr, Richard M. Sharpe
It is now accepted that normal testicular function is dependent upon multiple interactions between all of the different cell types in the testis.1–3 Potentially, one of the most important of these interactions is that between the Sertoli and Leydig cells, because it is the latter that supply the testosterone which acts on the Sertoli cells to drive spermatogenesis. Because of the dependence of spermatogenesis, and hence fertility, on an adequate supply of testosterone by the Leydig cells to the Sertoli cells, it is not surprising that several mechanisms have been shown to exist via which the Sertoli cells can exert paracrine control of the Leydig cells.1–3 In addition, it is now recognized that the Leydig cells are the source of at least two other hormones, oxytocin and opiates such as β-endorphin,1 the former of which acts on the peritubular myoid cells4 and the latter on the Sertoli cells.5 Multiple feedback signals may, therefore, be generated by the Sertoli cells to control the secretion of one or more of these Leydig cell products.
Hormonal regulation of spermatogenesis
Published in Rajender Singh, Molecular Signaling in Spermatogenesis and Male Infertility, 2019
Pallav Sengupta, Mohamed Arafa, Haitham Elbardisi
Testis, being an endocrine-responsive tissue, needs pristine cell-cell interactions to regulate cellular growth and differentiation. Sertoli cells in the seminiferous tubules confer cyto-architectural support and a proper microenvironment for sperm to develop. Peritubular myoid cells encase the seminiferous tubule. Networks of extracellular matrix separate them from the basal surface of the Sertoli cells. Leydig cells are present in the interstitium of the testis and are involved in androgen synthesis. Testicular cell-cell interactions primarily showcase the interactions among the Sertoli, Leydig, peritubular and germinal cells. However, there are other cell types that contribute to the proper reproductive functioning, including steroidogenesis and spermatogenesis. Cells such as the lymphatic endothelial, stromal cells, testicular macrophages, lymphocytes, etc., are involved in local cell-cell interactions, but their associations are yet to be elaborately revealed (8).
Cytoskeletons (F-actin) and spermatogenesis
Published in C. Yan Cheng, Spermatogenesis, 2018
Liza O’Donnell, Peter G. Stanton
The seminiferous tubules are surrounded by one or more continuous layers of peritubular myoid cells.96 These cells facilitate the contraction of seminiferous tubules to propel sperm and fluid along the tubules toward the rete testis.96 Consistent with their contractile nature, peritubular myoid cells contain layers of actin filaments (along with myosin motors) oriented in different directions (longitudinal and circular) in rodent97,98 and human testis.99 Contraction of the peritubular myoid cells is accompanied by marked rearrangements in the F-actin cytoskeleton,100 highlighting the fact that F-actin dynamics are important for seminiferous tubule contractility.
3D bioprinting for organ and organoid models and disease modeling
Published in Expert Opinion on Drug Discovery, 2023
Amanda C. Juraski, Sonali Sharma, Sydney Sparanese, Victor A. da Silva, Julie Wong, Zachary Laksman, Ryan Flannigan, Leili Rohani, Stephanie M. Willerth
In 2019, prepubertal human testicular cells from 2 patients (aged 6-months and 5 years old) were shown to form organoids with an organized basement membrane structure [61]. Using centrifugation, the authors formed aggregates of ~ 500 testicular cells each which were cultured for 5 days in supplemented media. While this study is the only article to our knowledge that has produced a basement membrane in vitro, the basement membrane was found on the surface of the spherical organoids, separating the luminal peritubular myoid cells from the surface-level Sertoli cells, suggesting reverse polarization of the Sertoli cells and organization. Future optimization of the cellular organization, reliable formation of the blood-testis barrier, and access to the luminal and interstitial interfaces may yield highly reliable constructs to apply screening for drug or environmental toxicities, gain of function with various factors, or even CRISPR-based screening protocols for mechanistic insight of spermatogenic or testicular cell function.
Immunohistochemical examination of androgen receptor and estrogen receptor alpha expressions in obstructive and non-obstructive azoospermia
Published in Systems Biology in Reproductive Medicine, 2021
Yurdun Kuyucu, Gülfidan Coşkun, Dilek Şaker, Özdem Karaoğlan, İbrahim Ferhat Ürünsak, Volkan İzol, İbrahim Atilla Arıdoğan, Şeyda Erdoğan, Hülya Özgür, Sait Polat
Testosterone shows its physiological actions via AR. AR expression has been reported in Sertoli, Leydig, peritubular myoid, spermatogenic, and vascular smooth muscle cells of the testis (Collins et al. 2003). AR gene is localized on the X chromosome. AR mutations are reported to result in androgen insensitivity syndrome and testicular feminization. AR knockout mice also revealed similar phenotypes to these disorders. Spermatogenesis arrest is reported in AR knockout mice (Wang et al. 2009). Decreased AR expression in Sertoli and peritubular myoid cells in NOA groups exemplifies the importance of AR in spermatogenesis. Genetic disorders, structural or molecular disorders of the AR, may reflect subtypes of the receptor reconciling the decreased AR immunoreactivity. Clarification of the reasons leading to decreased AR expression could enhance our understanding of NOA etiopathogenesis.
Spermatogonial stem cell transplantation and male infertility: Current status and future directions
Published in Arab Journal of Urology, 2018
Connor M. Forbes, Ryan Flannigan, Peter N. Schlegel
SSCs interact with their surrounding environment in the seminiferous compartment, but also receive signals from the testicular interstitium that may influence spermatogenic function [20]. The androgen receptor protein is expressed by foetal gonocytes and is thought to respond to Leydig cell secreted testosterone to suppress proliferation [20]. Testicular macrophages may influence SSCs through direct or indirect signalling pathways [20]. Peritubular myoid cells may also play a contributory role, possibly through androgen receptor activation and GDNF signalling to SSCs [20].