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Changes in Sertoli Cell Structure and Function
Published in Tom O. Abney, Brooks A. Keel, The Cryptorchid Testis, 2020
David M. de Kretser, Gail P. Risbridger
The past decade has witnessed a dramatic increase in our knowledge of the structure and function of the Sertoli cell (for reviews, see References 1 and 2). The pioneering ultrastructural studies established that each Sertoli cell is a distinct cellular entity and not a syncytium. However, subsequent studies have identified that specialized inter-Sertoli cell junctions exist which may facilitate cell-to-cell communication as well as forming the structural basis for the blood-testis barrier.1,3 The radial orientation of the Sertoli places it in a unique position to influence the environment of a number of different germ cell types since all germ cells, other than spermatogonia, are surrounded by processes of Sertoli cells. This dependence is heightened by the inter-Sertoli cell junctions which prevent intercellular transport of substances into the luminal region of the seminiferous epithelium. Thus, the centrally placed germ cells depend on the Sertoli cells for transport of nutrient materials.
Chromosome Pairing and Fertility in Mice
Published in Christopher B. Gillies, Fertility and Chromosome Pairing: Recent Studies in Plants and Animals, 2020
The effects of a lack of meiotic pairing on germ cell fate are thought to be rather independent of the region(s) of the genome it concerns. One exception to this rule could be constructed from the observations presented in this chapter when the two largely identical insertions Is(7;1)40H and Is(In7; X)lCt are compared. The former, unlike all other male-sterile chromosome syndromes, leads to a truncation of spermatogenesis at stage IV of the cycle of the seminiferous epithelium (see Figure 1). The latter, however, is the mildest of the X-autosome rearrangements, with appreciable numbers of spermatozoa and occasional fertility. As their distal breakpoints in chr 7 are approximately the same, this effect could be due to the segment 7B1–7C harboring a gene (or genes) that is (are) dependent on meiotic pairing for proper functioning. However, it could equally well be argued that the location of the “unpaired” chr 7 insertion is the prime cause for the contrast. In Is1Ct, the location is X-chromosomal in an area which normally never pairs. One might suppose that some of the tolerance of this area to absence of pairing is conveyed to the autosomal segment.
mTOR signaling in spermatogenesis and male infertility
Published in Rajender Singh, Molecular Signaling in Spermatogenesis and Male Infertility, 2019
The seminiferous epithelium consists of Sertoli cells that provide structural, functional and metabolic support to the developing germ cells. These cells are well ordered according to the developmental stages of germ cells and extend from the basement membrane to the lumen of the seminiferous tubule. Adjacent Sertoli cells form tight junctions or a blood-testis barrier (BTB) to divide the seminiferous tubule lumen into basal and adluminal compartments. During spermatogenesis, preleptotene spermatocytes are actively transported through this barrier to reach the adluminal compartment. The process of preleptotene spermatocyte transport is strictly coordinated and regulated through multiple signaling pathways without compromising the functional integrity of BTB. Several studies have reported that mTOR signaling regulates the dynamics of BTB remodeling, which facilitates the transport of preleptotene spermatocyte across the BTB (4,5). During spermatogenesis, the balance between self-renewal and differentiation of SSCs and the maintenance of BTB are two crucial events that are critically regulated by mTOR signaling. Any alteration in these events may lead to male infertility.
Microarray profiling of LncRNA expression in the testis of pubertal mice following morning and evening exposure to 1800 MHz radiofrequency fields
Published in Chronobiology International, 2021
Fenju Qin, Honglong Cao, Chuhan Feng, Tianyuan Zhu, Bingxu Zhu, Jie Zhang, Jian Tong, Hailong Pei
Hematoxylin-eosin (HE) staining results for testis acquired from the sham and RF groups mice are presented in Figure 2(a). In the sham groups, the seminiferous tubules within the testis showed good development; the diameter of the tubules was normal, there was good integration of the seminiferous epithelium, and evidence of normal spermatogenesis. The Leydig cells within the seminiferous tubules are normal in terms of their development and number. Following RF treatment, we observed that there was significant damage to the development of the seminiferous tubules and spermatogenesis. The diameter of the seminiferous tubule was smaller, and there was a lower number of cells in the seminiferous epithelium including (spermatogenic cells and sperm); there was also a lower number of Leydig cells that were also more immature. It was also evident that the extent of damage caused by exposure to RF in the morning (CT7:00) and the evening (CT19:00) showed marked changes. For example, mice that had been exposed to RF in the morning had no sperm cells and no mature sperm.
Common markers of testicular Sertoli cells
Published in Expert Review of Molecular Diagnostics, 2021
Xu You, Qian Chen, Ding Yuan, Changcheng Zhang, Haixia Zhao
VIM belongs to type III of the intermediate filaments family, and is the primary intermediate filament that constitutes the cellular cytoskeleton. In the testis [9], VIM is observed around the nuclei, along fibrillary material within the cytoplasm, and at the ectoplasmic specializations of Sertoli cell junctions – as well as throughout the periphery of the Sertoli cell processes – and plays an important role in anchoring germ cells to the seminiferous epithelium so as to maintain normal spermatogenesis [186,187]. Furthermore, VIM that is regularly expressed in Sertoli cells is independent of spermatogenic impairment or the state of Sertoli cell differentiation [12], such that VIM is still present in the Sertoli cells after treatment with some exogenous toxicants. However, its presence is completely disorganized within the seminiferous epithelium, being distributed non-homogeneously throughout the basal region of the Sertoli cells [188]. Intriguingly, VIM is increased in Sertoli cells in adult rhesus monkeys with cryptorchidism and in elderly men [9,186]. Collectively, the altered distribution of VIM has often been used as one of the parameters to identify abnormal spermatogenic states [188,189]. Therefore, VIM is also considered a marker of Sertoli cell configuration or a molecular marker of Sertoli cell surfaces, including the periphery and junctions [187,190].
Aluminum reproductive toxicity: a summary and interpretation of scientific reports
Published in Critical Reviews in Toxicology, 2020
The testes (singular testis) have two primary functions, to produce sperm and hormones including testosterone. The testes are composed of multiple seminiferous tubules and interstitial tissue, housed within a fibrous covering, the tunica albuginea. During embryonic development within the seminiferous germinal epithelium, Sertoli cells, which surround the developing germ cells, associate with the latter to form seminiferous tubules after birth. The seminiferous tubules are coiled masses that produce sperm cells through spermatogenesis, the maturation of germ cells to haploid spermatozoa. At birth, the seminiferous tubules contain spermatogonial stem cells. During the first round of spermatogenesis, Sertoli cells join to form tight junctions that compartmentalize the seminiferous epithelium into basal and luminal compartments. Spermatogonia, which are in the basal compartment, divide into type A spermatogonia that remain to replenish the precursor cells or type B spermatogonia. The latter, through meiosis in the luminal compartment, become (primary) spermatocytes. These divide to form secondary spermatocytes which meiotically divide to from spermatids, which are initially round. Multinucleated giant cells in the seminiferous tubules are degenerating germ cells. Spermatids become spermatozoa during late spermatogenesis.