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Journal articles on the topic 'Sertoli cell'

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Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

Iliadou, Paschalia, Christos Tsametis, Athina Kaprara, Ioannis Papadimas, and Dimitrios Goulis. "The Sertoli cell: Novel clinical potentiality." HORMONES 14, no. 4 (October 15, 2015): 504–14. http://dx.doi.org/10.14310/horm.2002.1648.

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2

de, Kretser DM. "Germ cell-Sertoli cell interactions." Reproduction, Fertility and Development 2, no. 3 (1990): 225. http://dx.doi.org/10.1071/rd9900225.

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The interactions between the Sertoli cells and germ cells are progressively becoming an important part of testicular physiology. This paper explores the cytological basis for these interactions, detailing the cyclic changes in the Sertoli cells in concert with the stages of the seminiferous cycle and the nature of the blood-testis barrier. These cytological changes are correlated with a number of variations in the function of Sertoli cells. The mechanisms by which germ cells and Sertoli cells interact are explored and can be divided into those using cell-to-cell contact and others utilizing paracrine factors.

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3

NISTAL, M., F. JIMENEZ, and R. PANIAGUA. "Sertoli cell types in the Sertoli-cell-only syndrome: relationships between Sertoli cell morphology and aetiology." Histopathology 16, no. 2 (April 3, 2007): 173–80. http://dx.doi.org/10.1111/j.1365-2559.1990.tb01086.x.

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4

Scialli, Anthony R. "The sertoli cell." Reproductive Toxicology 9, no. 2 (March 1995): 211–13. http://dx.doi.org/10.1016/s0890-6238(99)80005-7.

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5

Tsai, Robert Y. L. "SERTOLI CELL BIOLOGY." In Vitro Cellular & Developmental Biology - Animal 41, no. 5 (2005): 177. http://dx.doi.org/10.1290/br030501.1.

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6

Hadley, M. A., S. W. Byers, C. A. Suárez-Quian, H. K. Kleinman, and M. Dym. "Extracellular matrix regulates Sertoli cell differentiation, testicular cord formation, and germ cell development in vitro." Journal of Cell Biology 101, no. 4 (October 1, 1985): 1511–22. http://dx.doi.org/10.1083/jcb.101.4.1511.

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Sertoli cell preparations isolated from 10-day-old rats were cultured on three different substrates: plastic, a matrix deposited by co-culture of Sertoli and peritubular myoid cells, and a reconstituted basement membrane gel from the EHS tumor. When grown on plastic, Sertoli cells formed a squamous monolayer that did not retain contaminating germ cells. Grown on the matrix deposited by Sertoli-myoid cell co-cultures, Sertoli cells were more cuboidal and supported some germ cells but did not allow them to differentiate. After 3 wk however, the Sertoli cells flattened to resemble those grown on plastic. In contrast, the Sertoli cells grown on top of the reconstituted basement membrane formed polarized monolayers virtually identical to Sertoli cells in vivo. They were columnar with an elaborate cytoskeleton. In addition, they had characteristic basally located tight junctions and maintained germ cells for at least 5 wk in the basal aspect of the monolayer. However, germ cells did not differentiate. Total protein, androgen binding protein, transferrin, and type I collagen secretion were markedly greater when Sertoli cells were grown on the extracellular matrices than when they were grown on plastic. When Sertoli cells were cultured within rather than on top of reconstituted basement membrane gels they reorganized into cords. After one week, tight junctional complexes formed between adjacent Sertoli cells, functionally compartmentalizing the cords into central (adluminal) and peripheral (basal) compartments. Germ cells within the cords continued to differentiate. Thus, Sertoli cells cultured on top of extracellular matrix components assume a phenotype and morphology more characteristic of the in vivo, differentiated cells. Growing Sertoli cells within reconstituted basement membrane gels induces a morphogenesis of the cells into cords, which closely resemble the organ from which the cells were dissociated and which provide an environment permissive for germ cell differentiation.

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7

GROOTEGOED, J. ANTON, PIET J. DEN BOER, and PETRA MACKENBACH. "Sertoli Cell-Germ Cell Communication." Annals of the New York Academy of Sciences 564, no. 1 Regulation of (July 1989): 232–42. http://dx.doi.org/10.1111/j.1749-6632.1989.tb25900.x.

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8

Benahmed, M., J. Reventos, E. Tabone, and J. M. Saez. "Cultured Sertoli cell-mediated FSH stimulatory effect on Leydig cell steroidogenesis." American Journal of Physiology-Endocrinology and Metabolism 248, no. 2 (February 1, 1985): E176—E181. http://dx.doi.org/10.1152/ajpendo.1985.248.2.e176.

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To determine the precise role of Sertoli cells in the stimulating effects of follicle stimulating hormone (FSH) on Leydig cell activity, porcine purified Leydig and Sertoli cells were cultured separately or together in a chemically defined medium in the absence or presence of porcine, FSH 50 ng/ml. Leydig cell activity was evaluated using two parameters: human chorionic gonadotropin (hCG) binding sites; and hCG-stimulated cAMP production and testosterone secretion. First, it was found that FSH increases Leydig cell activity in crude Leydig cell preparations (40–60% of Leydig cells), whereas it exerts no effect on purified Leydig cells (greater than 90% of Leydig cells). Second, FSH stimulates the activity of Leydig cells cocultured with Sertoli cells, whereas it remains without effect on purified Leydig cells cultured alone. This stimulating effect of FSH on Leydig cell activity is dependent on the Sertoli cell number in the coculture. These data 1) show that the stimulating effect of FSH on Leydig cell function is mediated by Sertoli cells and 2) support the concept of local control of Leydig cell function originating from Sertoli cells.

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9

Halder, Ashutosh, and Manish Jain. "Sertoli cell only syndrome: Status of sertoli cell maturation and function." Indian Journal of Endocrinology and Metabolism 16, no. 8 (2012): 512. http://dx.doi.org/10.4103/2230-8210.104154.

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10

Fatima, Arooj, Sajid Mushtaq, and Asif Loya. "Expression of NKX 3.1 in Sertoli Cell Tumors." Pakistan Armed Forces Medical Journal 72, no. 6 (December 29, 2022): 1965–68. http://dx.doi.org/10.51253/pafmj.v72i6.6430.

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Objective: To evaluate the NKX3.1 expression by immunohistochemistry in normal testicular parenchyma and in Sertoli cell tumours and Sertoli Leydig cell tumours of the testes and ovary. Study Design: Retrospective longitudinal study. Place and Duration of Study: Shaukat Khanum Memorial Cancer Hospital and Research Centre, Lahore Pakistan, from 2010-2021. Methodology: We used immunohistochemistry to evaluate the positivity and loss of nuclear expression of NKX3.1 in the Sertoli cell tumour (11 cases), Sertoli Leydig cell tumour (31 cases) and in normal testicular parenchyma (7 cases). Results: In our study, there were 49 cases. All the cases of benign testicular parenchyma expressed positivity with nuclear staining of NKX 3.1 in Sertoli cells. Two out of 11 Sertoli cell tumours expressed positivity with nuclear positivity of NKX 3.1 in Sertoli cell component (18.18%) and 9 of the cases showed loss of staining of NKX 3.1 (81.8%). All Sertoli Leydig cell tumours showed loss of staining of NKX 3.1. Conclusion: Nuclear expression of NKX 3.1 is seen in Sertoli cells of normal testicular parenchyma. This staining is lost in Sertoli cell tumours and Sertoli Leydig cell tumours.

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11

Guigon, Céline J., Noëlline Coudouel, Séverine Mazaud-Guittot, Maguelone G. Forest, and Solange Magre. "Follicular Cells Acquire Sertoli Cell Characteristics after Oocyte Loss." Endocrinology 146, no. 7 (July 1, 2005): 2992–3004. http://dx.doi.org/10.1210/en.2005-0045.

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Abstract Although it has been suggested that in mammals the loss of female germ cells may induce the masculinization of the ovarian compartment, there has been as yet no conclusive demonstration. To directly address that question, the present study has been designed to determine the fate of follicular cells after oocyte loss. Using γ-irradiation to selectively deplete oocytes in nongrowing follicles in female rats, we show that follicular cells in oocyte-depleted follicles survive, proliferate, and subsequently acquire morphological characteristics of Sertoli cells: elongated cytoplasm, basal location of the nucleus, and specific Sertoli cell junctions, the ectoplasmic specializations. These Sertoli-like cells express, however, the female-specific marker FOXL2 (Forkhead L2) but not the male sex-specific marker SOX-9 (Sry-type high-mobility-group box transcription factor-9) underlying the maintenance of molecular characteristics of granulosa cells. Before transdifferentiating into Sertoli-like cells, follicular cells of oocyte-depleted follicles initiate the expression of anti-Mullerian hormone and inhibin α-subunit that are typically synthesized by granulosa cells from the onset of follicular growth. Experimental modifications of the endocrine balance of the irradiated females show that there is a close relationship between plasma FSH levels and the occurrence of Sertoli-like cells. In addition to providing experimental evidence for the crucial role of the oocyte in granulosa cell phenotype maintenance, these results emphasize that the transdifferentiation of granulosa cells into Sertoli cells occurs in a multistep fashion, requiring the maturation of granulosa cells and depending on the endocrine milieu.

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12

Eusebi, Fabrizio, Francesca Grassi, Guiseppe Fratamico, Susanna Dolci, Marco Conti, and Mario Stefanini. "Cell-to-cell communication in cultured Sertoli cells." Pfl�gers Archiv European Journal of Physiology 404, no. 4 (August 1985): 382–84. http://dx.doi.org/10.1007/bf00585353.

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13

FRANCHI, E., and M. CAMATINI. "Morphological evidence for calcium stores at Sertoli-Sertoli and Sertoli-spermatid interrelations." Cell Biology International Reports 9, no. 5 (May 1985): 441–46. http://dx.doi.org/10.1016/0309-1651(85)90152-3.

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14

Abel, M. H., P. J. Baker, H. M. Charlton, A. Monteiro, G. Verhoeven, K. De Gendt, F. Guillou, and P. J. O’Shaughnessy. "Spermatogenesis and Sertoli Cell Activity in Mice Lacking Sertoli Cell Receptors for Follicle-Stimulating Hormone and Androgen." Endocrinology 149, no. 7 (April 10, 2008): 3279–85. http://dx.doi.org/10.1210/en.2008-0086.

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Spermatogenesis in the adult male depends on the action of FSH and androgen. Ablation of either hormone has deleterious effects on Sertoli cell function and the progression of germ cells through spermatogenesis. In this study we generated mice lacking both FSH receptors (FSHRKO) and androgen receptors on the Sertoli cell (SCARKO) to examine how FSH and androgen combine to regulate Sertoli cell function and spermatogenesis. Sertoli cell number in FSHRKO-SCARKO mice was reduced by about 50% but was not significantly different from FSHRKO mice. In contrast, total germ cell number in FSHRKO-SCARKO mice was reduced to 2% of control mice (and 20% of SCARKO mice) due to a failure to progress beyond early meiosis. Measurement of Sertoli cell-specific transcript levels showed that about a third were independent of hormonal action on the Sertoli cell, whereas others were predominantly androgen dependent or showed redundant control by FSH and androgen. Results show that FSH and androgen act through redundant, additive, and synergistic regulation of spermatogenesis and Sertoli cell activity. In addition, the Sertoli cell retains a significant capacity for activity, which is independent of direct hormonal regulation.

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15

Gerard, N., A. Corlu, B. Kneip, H. Kercret, M. Rissel, C. Guguen-Guillouzo, and B. Jegou. "Liver-regulating protein (LRP) is a plasma membrane protein involved in cell contact-mediated regulation of Sertoli cell function by primary spermatocytes." Journal of Cell Science 108, no. 3 (March 1, 1995): 917–25. http://dx.doi.org/10.1242/jcs.108.3.917.

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We have identified a liver-regulating protein involved in cell contact-mediated regulation of Sertoli cell function by primary spermatocytes in rat testis. Liver-regulating protein was studied using monoclonal antibody L8 prepared from rat primitive biliary epithelial cells. This molecule was located in vivo at the interface of Sertoli cells and spermatocytes, and expressed in a stage-dependent manner (expression peaked on leptotene-zygotene spermatocytes). In vitro, the liver-regulating protein was found on Sertoli cell, spermatocyte and early spermatid membranes. Immunoaffinity procedures revealed two peptides of 85 and 73 kDa for Sertoli cells, while spermatocytes and spermatids displayed a single smaller peptide of 56 kDa. The involvement of the liver-regulating protein in cell interaction-mediated regulation of Sertoli cell was assessed in vitro by tracing Sertoli cell transferrin and inhibin secretion, as well as mRNA synthesis in spermatocyte-Sertoli cell cocultures and in rat liver biliary epithelial cell-Sertoli cell cocultures, performed in the presence or absence of monoclonal antibody L8. Inhibition of the spermatocyte- and liver biliary epithelial cell-stimulated secretion of transferrin and inhibin by Sertoli cells was observed in the presence of antibody, whereas spermatocyte adhesiveness was unchanged. Using northern blot analysis, the steady state levels of transferrin mRNA decreased when the anti-liver-regulating protein antibody was added to the Sertoli cell-spermatocyte cocultures or to the Sertoli cell-liver biliary epithelial cell cocultures. The data demonstrate the role of the liver-regulating protein in cell-cell contact-mediated regulation of Sertoli function by primary spermatocytes and the important implications of this cell contact-dependent control in testicular activity.

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16

ŞENGİZ ERHAN, Selma, Ayşe Tülay SAYILGAN, Servet ŞİŞMAN, Deniz ÖZCAN, and Simten GENÇ. "Sertoli-Leydig Cell Tumor." Turkiye Klinikleri Journal of Case Reports 27, no. 4 (2019): 185–91. http://dx.doi.org/10.5336/caserep.2019-65443.

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17

Khouzam, M. N. "Sertoli Leydig cell tumours." Journal of Obstetrics and Gynaecology 7, no. 2 (October 1, 1986): 147–48. http://dx.doi.org/10.3109/01443618609112302.

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18

Khouzam, M. N. "Sertoli Leydig cell tumours." Journal of Obstetrics and Gynaecology 7, no. 3 (January 1987): 147–48. http://dx.doi.org/10.3109/01443618709068496.

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19

Vallangeon, Bethany D., John N. Eble, and Thomas M. Ulbright. "Macroscopic Sertoli Cell Nodule." American Journal of Surgical Pathology 34, no. 12 (December 2010): 1874–80. http://dx.doi.org/10.1097/pas.0b013e3181fcab70.

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20

Smith, Steven C., Serguei I. Bannykh, and Mahul B. Amin. "Melanotic Sertoli Cell Tumor." American Journal of Surgical Pathology 38, no. 9 (September 2014): 1305–6. http://dx.doi.org/10.1097/pas.0000000000000281.

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21

SAEZ, J. M., O. AVALLET, D. NAVILLE, M. H. PERRARD-SAPORI, and P. G. CHATELAIN. "Sertoli-Leydig Cell Communications." Annals of the New York Academy of Sciences 564, no. 1 Regulation of (July 1989): 210–31. http://dx.doi.org/10.1111/j.1749-6632.1989.tb25899.x.

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22

Jégou, Bernard. "3 The sertoli cell." Baillière's Clinical Endocrinology and Metabolism 6, no. 2 (April 1992): 273–311. http://dx.doi.org/10.1016/s0950-351x(05)80151-x.

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23

Hovatta, O. "Sertoli cell only syndrome." Human Reproduction 11, no. 1 (January 1, 1996): 229. http://dx.doi.org/10.1093/oxfordjournals.humrep.a019025.

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24

Silber, Sherman J., André C. Van Steirteghem, and Paul Devroey. "Sertoli cell only revisited." Human Reproduction 10, no. 5 (May 1995): 1031–32. http://dx.doi.org/10.1093/oxfordjournals.humrep.a136085.

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25

Lantzsch, T., S. Stoerer, K. Lawrenz, J. Buchmann, H. G. Strauss, and H. Koelbl. "Sertoli-Leydig cell tumor." Archives of Gynecology and Obstetrics 264, no. 4 (January 26, 2001): 206–8. http://dx.doi.org/10.1007/s004040000114.

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26

Guan, Yongjuan, Guanxiang Liang, Penny A. R. Hawken, Sarah J. Meachem, Irek A. Malecki, Seungmin Ham, Tom Stewart, Le Luo Guan, and Graeme B. Martin. "Nutrition affects Sertoli cell function but not Sertoli cell numbers in sexually mature male sheep." Reproduction, Fertility and Development 28, no. 8 (2016): 1152. http://dx.doi.org/10.1071/rd14368.

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We tested whether the reversible effects of nutrition on spermatogenesis in sexually mature sheep were mediated by Sertoli cells. Rams were fed with diets designed to achieve a 10% increase (High), no change (Maintenance) or a 10% decrease (Low) in body mass after 65 days. At the end of treatment, testes were lighter in the Low than the High group (P < 0.01). The Maintenance group had intermediate values that were not significantly different from those of the other two groups. Spermatogenesis (Johnsen score) was impaired in the Low group, but normal in both other groups. There was no effect of treatment on Sertoli cell numbers, although 1% of Sertoli cells appeared to retain their ability to proliferate. By contrast, Sertoli cell function was affected by dietary treatment, as evidenced by differences between the High and Low groups (P < 0.05) in the expression of seven Sertoli cell-specific genes. Under-nutrition appeared to reverse cellular differentiation leading to disruption of tight-junction morphology. In conclusion, in sexually mature sheep, reversible reductions in testis mass and spermatogenesis caused by under-nutrition were associated with impairment of basic aspects of Sertoli cell function but not with changes in the number of Sertoli cells.

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27

Silber, S. J. "Sertoli cell only>Letters to the Editor: Sertoli cell only syndrome." Human Reproduction 11, no. 1 (January 1, 1996): 229. http://dx.doi.org/10.1093/oxfordjournals.humrep.a019026.

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28

Sun, Hongyan, Guomin Zhang, Fulu Dong, Feng Wang, and Wenguang Cao. "Reprogramming Sertoli Cells into Pluripotent Stem Cells." Cellular Reprogramming 16, no. 3 (June 2014): 196–205. http://dx.doi.org/10.1089/cell.2013.0083.

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29

Cameron, D. F., and K. E. Muffly. "Hormonal regulation of spermatid binding." Journal of Cell Science 100, no. 3 (November 1, 1991): 623–33. http://dx.doi.org/10.1242/jcs.100.3.623.

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A Sertoli-spermatid coculture model is described in which a large percentage (greater than 76%) of round spermatids remain viable for 48 h and bind to Sertoli cells. The effects of follicle-stimulating hormone (FSH) and testosterone on spermatid binding (expressed as the spermatid density; SD = the number of spermatids per unit area of Sertoli cell cytoplasm), ultrastructure of the Sertoli-spermatid junctional complex, and distribution in the Sertoli cell of junction-related F-actin and vinculin are described. Following 48 h of incubation, neither FSH alone nor testosterone alone affected spermatid binding to Sertoli cells beyond that observed in control cocultures. However, the combination of FSH and testosterone (FSH + testosterone) resulted in a significant increase in the density of spermatids bound to Sertoli cells. Junction-related structure of the Sertoli cell cytoskeleton between the Sertoli cell and the pre-step 8 spermatid was different than that observed between the Sertoli cell and the post-step 8 spermatid. The junction-related cytoskeletal modification of the Sertoli cell (JCMS) in the latter was similar in appearance to the well-described ‘Sertoli ectoplasmic specialization’ observed adjacent to post-step 8 spermatids in vivo. FSH + testosterone and FSH alone, but not testosterone alone, resulted in the peripheral distribution of actin and vinculin, which otherwise remained in stress fiber-like structures throughout the Sertoli cell. Results show that maximal spermatid binding to Sertoli cells in vitro requires FSH + testosterone and is associated with the peripheral distribution of actin and vinculin.

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30

Dufour, Jannette M., Brinda Dass, Katie R. Halley, Gregory S. Korbutt, Doreen E. Dixon, and Ray V. Rajotte. "Sertoli Cell Line Lacks the Immunoprotective Properties Associated with Primary Sertoli Cells." Cell Transplantation 17, no. 5 (May 2008): 525–34. http://dx.doi.org/10.3727/096368908785096033.

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31

Rebourcet, Diane, Peter J. O'Shaughnessy, and Lee B. Smith. "The expanded roles of Sertoli cells: lessons from Sertoli cell ablation models." Current Opinion in Endocrine and Metabolic Research 6 (June 2019): 42–48. http://dx.doi.org/10.1016/j.coemr.2019.04.003.

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32

Benbrahim-Tallaa, Lamia, Bénazir Siddeek, Aline Bozec, Virginie Tronchon, Anne Florin, Claire Friry, Eric Tabone, Claire Mauduit, and Mohamed Benahmed. "Alterations of Sertoli cell activity in the long-term testicular germ cell death process induced by fetal androgen disruption." Journal of Endocrinology 196, no. 1 (October 10, 2007): 21–31. http://dx.doi.org/10.1677/joe-07-0062.

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Fetal androgen disruption, induced by the administration of anti-androgen flutamide (0.4, 2, and 10 mg/kg day) causes a long-term apoptosis in testicular germ cells in adult male rat offspring. One of the questions raised by this observation is the role of the Sertoli cells in the adult germ cell apoptotic process. It is shown here that Sertoli cells originating from 15-day-old rats treated in utero with the anti-androgen (10 mg/kg d) did no longer protect adult germ cells against apoptosis. Indeed, untreated spermatocytes or spermatids exhibited increased (P<0.0001) active caspase-3 levels when co-cultured with Sertoli cells isolated from rat testes exposed in utero to the anti-androgen. This alteration of Sertoli cell functions was not due to modifications in the androgen signal in the adult (90-day-old) animals, since plasma testosterone and estradiol, androgen receptor expression, and androgen-targeted cell number (e.g., Sertoli cells in the seminiferous tubules) were not affected by the fetal androgen disruption. In contrast, this inability of Sertoli cells to protect germ cells against apoptosis could be accounted for by the potential failure of Sertoli cell functions. Indeed, adult testes exposed in utero to anti-androgens displayed decreased levels of several genes mainly expressed in adult Sertoli cells (anti-Mullerian hormone receptor type II (AMHR2), Cox-1, cyclin D2, cathepsin L, and GSTα). In conclusion, fetal androgen disruption may induce alterations of Sertoli cell activity probably related to Sertoli cell maturation, which potentially leads to increased adult germ cell apoptosis.

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33

Dong, Heling, Zhenguo Chen, Caixia Wang, Zhi Xiong, Wanlu Zhao, Chunhong Jia, Jun Lin, et al. "Rictor Regulates Spermatogenesis by Controlling Sertoli Cell Cytoskeletal Organization and Cell Polarity in the Mouse Testis." Endocrinology 156, no. 11 (September 11, 2015): 4244–56. http://dx.doi.org/10.1210/en.2015-1217.

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Maintenance of cell polarity is essential for Sertoli cell and blood-testis barrier (BTB) function and spermatogenesis; however, the signaling mechanisms that regulate the integrity of the cytoskeleton and polarity of Sertoli cells are not fully understood. Here, we demonstrate that rapamycin-insensitive component of target of rapamycin (TOR) (Rictor), a core component of mechanistic TOR complex 2 (mTORC2), was expressed in the seminiferous epithelium during testicular development, and was down-regulated in a cadmium chloride-induced BTB damage model. We then conditionally deleted the Rictor gene in Sertoli cells and mutant mice exhibited azoospermia and were sterile as early as 3 months old. Further study revealed that Rictor may regulate actin organization via both mTORC2-dependent and mTORC2-independent mechanisms, in which the small GTPase, ras-related C3 botulinum toxin substrate 1, and phosphorylation of the actin filament regulatory protein, Paxillin, are involved, respectively. Loss of Rictor in Sertoli cells perturbed actin dynamics and caused microtubule disarrangement, both of which accumulatively disrupted Sertoli cell polarity and BTB integrity, accompanied by testicular developmental defects, spermiogenic arrest and excessive germ cell loss in mutant mice. Together, these findings establish the importance of Rictor/mTORC2 signaling in Sertoli cell function and spermatogenesis through the maintenance of Sertoli cell cytoskeletal dynamics, BTB integrity, and cell polarity.

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34

Cameron, D. F., J. J. Hushen, T. Dejarlais, L. Colado, K. M. Wolski, P. R. Sanberg, and S. Saporta. "A Unique Cytoplasmic Marker for Extratesticular Sertoli Cells." Cell Transplantation 11, no. 6 (September 2002): 507–12. http://dx.doi.org/10.3727/000000002783985530.

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In the absence of a definitive cell marker for testis-derived Sertoli cells, their identification in cell culture or in Sertoli cell-facilitated cell transplantation protocols is difficult and limits the creditable evaluation of experimental results. However, the production by prepubertal Sertoli cells of Mullerian inhibiting substance (MIS) presents the possibility of specifically identifying extratesticular Sertoli cells as well as Sertoli cells in situ, by the immunodection of this unique glycoprotein. This study was designed to determine if isolated rat Sertoli cells could be identified by routine immunocytochemistry utilizing an antibody raised against MIS. Sertoli cells immunostained for MIS included Sertoli cells in situ and freshly isolated, cultured and cocultured Sertoli cells, and Sertoli cells structurally integrated with NT2 cells in simulated microgravity. Detection of MIS was also determined by Western blot analysis.

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35

Al-Obaidy, Khaleel I., Muhammad T. Idrees, Eman Abdulfatah, Lakshmi P. Kunju, Angela Wu, and Thomas M. Ulbright. "Large Cell Calcifying Sertoli Cell Tumor." American Journal of Surgical Pathology 46, no. 5 (December 16, 2021): 688–700. http://dx.doi.org/10.1097/pas.0000000000001849.

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36

Redgrave, N. G., P. Allan, and W. F. Johnson. "Large cell calcifying Sertoli cell tumour." British Journal of Urology 75, no. 3 (March 1995): 411–12. http://dx.doi.org/10.1111/j.1464-410x.1995.tb07360.x.

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37

Buchino, Joseph J., John J. Buchino, and Eric R. Uhlenhuth. "Large-Cell Calcifying Sertoli Cell Tumor." Journal of Urology 141, no. 4 (April 1989): 953–54. http://dx.doi.org/10.1016/s0022-5347(17)41067-6.

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38

Wang, Shuai, Pengxiang Wang, Dongli Liang, and Yuan Wang. "BRG1 Is Dispensable for Sertoli Cell Development and Functions in Mice." International Journal of Molecular Sciences 21, no. 12 (June 19, 2020): 4358. http://dx.doi.org/10.3390/ijms21124358.

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Sertoli cells are somatic supporting cells in spermatogenic niche and play critical roles in germ cell development, but it is yet to be understood how epigenetic modifiers regulate Sertoli cell development and contribution to spermatogenesis. BRG1 (Brahma related gene 1) is a catalytic subunit of the mammalian SWI/SNF chromatin remodeling complex and participates in transcriptional regulation. The present study aimed to define the functions of BRG1 in mouse Sertoli cells during mouse spermatogenesis. We found that BRG1 protein was localized in the nuclei of both Sertoli cells and germ cells in seminiferous tubules. We further examined the requirement of BRG1 in Sertoli cell development using a Brg1 conditional knockout mouse model and two Amh-Cre mouse strains to specifically delete Brg1 gene from Sertoli cells. We found that the Amh-Cre mice from Jackson Laboratory had inefficient recombinase activities in Sertoli cells, while the other Amh-Cre strain from the European Mouse Mutant Archive achieved complete Brg1 deletion in Sertoli cells. Nevertheless, the conditional knockout of Brg1 from Sertoli cells by neither of Amh-Cre strains led to any detectable abnormalities in the development of either Sertoli cells or germ cells, suggesting that BRG1-SWI/SNF complex is dispensable to the functions of Sertoli cells in spermatogenesis.

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Haverfield, J. T., P. G. Stanton, and S. J. Meachem. "101. THE RELATIONSHIP BETWEEN SERTOLI CELL STATUS AND IDIOPATHIC MALE INFERTILITY." Reproduction, Fertility and Development 22, no. 9 (2010): 19. http://dx.doi.org/10.1071/srb10abs101.

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The cornerstone of normal adult testicular function is a mature Sertoli cell population. The maturational switch for Sertoli cells occurs at puberty, where immature Sertoli cells differentiate into a mature population that hold the necessary architectural and functional characteristics to regulate spermatogenesis (1). Data from rodent models (2, 3) suggest a relationship between Sertoli cell immaturity and infertility, however clinical data confirming this relationship is limited. We postulate that adult Sertoli cells in the infertile human testis display an immature status, with more severe disruptions of spermatogenesis associating with a greater extent of Sertoli cell immaturity. Using testicular biopsy samples obtained from fertile men (n = 3) and infertile patients (n = 6/group) displaying meiotic arrest (MA) and Sertoli cell only (SCO) syndrome, we sought to survey the status of Sertoli cell populations. All samples were immunofluorescently probed for three hallmark features of adult Sertoli cell maturation; organisation of the inter-Sertoli tight junctions, expression of the androgen receptor and proliferative ability. Differences between groups were quantified using stereology. The results show that the majority of infertile patients display highly disorganised tight junctions, a feature not seen in fertile men, however surprisingly no difference in the extent of tight junction disruption was observed between MA and SCO. Preliminary data also show that some component of the Sertoli cell population in MA and SCO patients was non-functional and proliferative. These results suggest that the Sertoli cell population in men suffering from idiopathic infertility present an abnormal maturational status that is independent of the extent of spermatogenic disruption. Moreover, this study supports the growing body of evidence proposing that the adult Sertoli cell population is not a homogenous, terminally differentiated population, and suggests that the failure of Sertoli cells to reach or maintain their mature status may be the cornerstone of abnormal adult testicular function. (1) Sharpe R.M. et al., 2003, Reproduction, 125: 769.(2) Tarulli G.A. et al., 2006, Biology of Reproduction, 74: 798–806.(3) Tarulli G.A. et al., 2008, Reproduction, 135: 867–877.

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Yan, Rong-Ge, Qi-Lin Yang, and Qi-En Yang. "E4 Transcription Factor 1 (E4F1) Regulates Sertoli Cell Proliferation and Fertility in Mice." Animals 10, no. 9 (September 18, 2020): 1691. http://dx.doi.org/10.3390/ani10091691.

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In the mammalian testes, Sertoli cells are the only somatic cells in the seminiferous tubules that provide structural, nutritional and regulatory support for developing spermatogenic cells. Sertoli cells only proliferate during the fetal and neonatal periods and enter a quiescent state after puberty. Functional evidences suggest that the size of Sertoli cell population determines sperm production and fertility. However, factors that direct Sertoli cell proliferation and maturation are not fully understood. Transcription factor E4F1 is a multifunctional protein that serves essential roles in cell fate decisions and because it interacts with pRB, a master regulator of Sertoli cell function, we hypothesized that E4F1 may have a functional role in Sertoli cells. E4f1 mRNA was present in murine testis and immunohistochemical staining confirmed that E4F1 was enriched in mature Sertoli cells. We generated a conditional knockout mouse model using Amh-cre and E4f1flox/flox lines to study E4F1 fucntion in Sertoli cells and the results showed that E4f1 deletion caused a significant reduction in testis size and fertility. Further analyses revealed that meiosis progression and spermiogenesis were normal, however, Sertoli cell proliferation was impaired and germ cell apoptosis was elevated in the testis of E4f1 conditional knockout mice. On the basis of these findings, we concluded that E4F1 was expressed in murine Sertoli cells and served important functions in regulating Sertoli cell proliferation and fertility.

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Nicholls, Peter K., Peter G. Stanton, Justin L. Chen, Justine S. Olcorn, Jenna T. Haverfield, Hongwei Qian, Kelly L. Walton, Paul Gregorevic, and Craig A. Harrison. "Activin Signaling Regulates Sertoli Cell Differentiation and Function." Endocrinology 153, no. 12 (December 1, 2012): 6065–77. http://dx.doi.org/10.1210/en.2012-1821.

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Abstract Throughout development, activin A signaling stimulates proliferation and inhibits differentiation of testicular Sertoli cells. A decline in activin levels at puberty corresponds with the differentiation of Sertoli cells that is required to sustain spermatogenesis. In this study, we consider whether terminally differentiated Sertoli cells can revert to a functionally immature phenotype in response to activin A. To increase systemic activin levels, the right tibialis anterior muscle of 7-wk-old C57BL/6J mice was transduced with an adeno-associated virus (rAAV6) expressing activin A. We show that chronic activin signaling reduces testis mass by 23.5% compared with control animals and induces a hypospermatogenic phenotype, consistent with a failure of Sertoli cells to support spermatogenesis. We use permeability tracers and transepithelial electrical resistance measurements to demonstrate that activin potently disrupts blood-testis-barrier function in adult mice and ablates tight junction formation in differentiated primary Sertoli cells, respectively. Furthermore, increased activin signaling reinitiates a program of cellular proliferation in primary Sertoli cells as determined by 5-ethynyl-2′-deoxyuridine incorporation. Proliferative cells reexpress juvenile markers, including cytokeratin-18, and suppress mature markers, including claudin-11. Thus, activin A is the first identified factor capable of reprogramming Sertoli cells to an immature, dedifferentiated phenotype. This study indicates that activin signaling must be strictly controlled in the adult in order to maintain Sertoli cell function in spermatogenesis.

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Chaudhary, Jaideep, Andrea S. Cupp, and Michael K. Skinner. "Role of Basic-Helix-Loop-Helix Transcription Factors in Sertoli Cell Differentiation: Identification of an E-Box Response Element in the Transferrin Promoter*." Endocrinology 138, no. 2 (February 1, 1997): 667–75. http://dx.doi.org/10.1210/endo.138.2.4942.

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Abstract Sertoli cells are critical for testicular function and maintenance of the spermatogenic process. The induction of Sertoli cell differentiation in the embryo promotes testicular development and male sex determination. The progression of Sertoli cell differentiation during puberty promotes the onset of spermatogenesis. The maintenance of optimal Sertoli cell differentiation in the adult is required for spermatogenesis to proceed. The current study was designed to investigate the transcriptional regulation of Sertoli cell differentiation through the analysis of a previously identified marker of differentiation, transferrin gene expression. Sertoli cells produce transferrin to transport iron to developing spermatogenic cells sequestered within the blood-testis barrier. The transferrin promoter was characterized and found to contain two critical response elements, designated Sertoli element 1 (SE1) and Sertoli element 2 (SE2). Through sequence analysis, SE2 was found to contain an E-box response element, which has been shown to respond to basic-helix-loop-helix (bHLH) transcription factors. The bHLH proteins are a class of transcription factors associated with the induction and progression of cell differentiation. bHLH proteins dimerize through the conserved helix-loop-helix region and bind DNA through the basic region. Nuclear extracts from Sertoli cells were found to cause an E-box gel shift when the cells were stimulated to differentiate in culture, but not under basal conditions. The SE2 gel shift of Sertoli nuclear extracts was competed with excess unlabeled SE2 or E-box DNA fragments. Several Sertoli nuclear proteins associate with the SE2 gel shifts, including 70-, 42-, and 25-kDa proteins. Therefore, the critical SE2 element in the transferrin promoter is an E-box element capable of binding bHLH transcription factors. The ubiquitously expressed E12 bHLH protein dimerizes with numerous cell-specific bHLH factors. A Western blot analysis demonstrated that E12 was present in Sertoli cell nuclear extracts and associated with the SE2 gel shift. A ligand blot of Sertoli cell nuclear extracts with radiolabeled E12 had apparent bHLH proteins when the cells were stimulated to differentiate. The E-box sequence in the SE2 fragment of the transferrin promoter was CATCTG and was similar in gel shifts to the consensus E-box elements (CANNTG) previously characterized. A bHLH inhibitory factor (Id) competed and inhibited formation of the Sertoli cell nuclear extract E-box gel shift. To extend this observation, Id protein was overexpressed in cultured Sertoli cells. A transferrin promoter chloramphenicol acetyltransferase construct was used to monitor Sertoli cell function. The presence of Id suppressed the activation of the promoter induced by Sertoli differentiation factors. Therefore, the inhibition of Sertoli bHLH factors by Id suppressed Sertoli cell differentiated function, as measured by transferrin expression. An E-box-chloramphenicol acetyltransferase construct was also found to be active in Sertoli cells when cells were induced to differentiate. Screening the computerized nucleotide data bases demonstrated that putative E-box response elements are present in the promoters of a large number of Sertoli cell differentiated genes. In summary, a critical E-box response element has been identified in the transferrin promoter that can be activated by bHLH factors (e.g. E12) present in Sertoli cells. Inhibition of Sertoli bHLH factors by Id suppresses Sertoli cell differentiated function (i.e. transferrin expression), suggesting that bHLH transcription factors may be important in regulating Sertoli cell differentiated functions.

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Camacho-Moll, Maria E., Leendert H. J. Looijenga, Roland Donat, Chitranjan J. Shukla, Anne Jørgensen, and Rod T. Mitchell. "Expression of Intermediate Filaments in the Developing Testis and Testicular Germ Cell Cancer." Cancers 14, no. 22 (November 8, 2022): 5479. http://dx.doi.org/10.3390/cancers14225479.

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Cytokeratin and desmin expression have been associated with Sertoli cell maturity and the development of testicular germ cell cancer (TGCC). Thus, the present study aimed to characterize the expression of these intermediate filaments in normal testis development and TGCC. Cytokeratin and desmin were determined by immunohistochemistry and immunofluorescence in human fetal, and adult testis and tissue from patients with pre-invasive germ cell neoplasia in-situ (GCNIS) or invasive TGCC. Desmin was expressed in Sertoli cells of the human fetal testis, and the proportion of desmin expressing Sertoli cells was significantly reduced in the second trimester, compared with the first trimester (31.14% vs. 6.74%, p = 0.0016). Additionally, Desmin was expressed in the majority of Sertoli cells in the adult testis and TGCC samples. Cytokeratin was detected in Sertoli cells of human fetal testis but was not expressed in Sertoli cells of human adult testis. In patients with TGCC, cytokeratin was not expressed in Sertoli cells in tubules with active spermatogenesis but was detected in Sertoli cells in tubules containing GCNIS cells in patients with both pre-invasive and invasive TGCC. In conclusion, desmin was not associated with Sertoli cell maturation or progression to TGCC. However, cytokeratin appeared to be an indicator of impaired Sertoli cell maturation.

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Barghorn, A., H.-R. Alioth, S. Hailemariam, F. Bannwart, and T. M. Ulbright. "Giant Sertoli cell nodule of the testis: distinction from other Sertoli cell lesions." Journal of Clinical Pathology 59, no. 11 (May 5, 2006): 1223–25. http://dx.doi.org/10.1136/jcp.2005.035253.

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Glenn McCluggage, W., and Robert H. Young. "Ovarian Sertoli-Leydig Cell Tumors With Pseudoendometrioid Tubules (Pseudoendometrioid Sertoli-Leydig Cell Tumors)." American Journal of Surgical Pathology 31, no. 4 (April 2007): 592–97. http://dx.doi.org/10.1097/01.pas.0000213365.56498.72.

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Enders, G. C., J. H. Henson, and C. F. Millette. "Sertoli cell binding to isolated testicular basement membrane." Journal of Cell Biology 103, no. 3 (September 1, 1986): 1109–19. http://dx.doi.org/10.1083/jcb.103.3.1109.

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We have examined the adhesion of primary Sertoli cells to a seminiferous tubule basement membrane (STBM) preparation in vitro. The STBM isolation procedure (Watanabe, T.K., L.J. Hansen, N.K. Reddy, Y.S. Kanwar, and J.K. Reddy, 1984, Cancer Res., 44:5361-5368) yields segments of STBM that retain their histotypic form in both three-dimensional tubular geometry and ultrastructural appearance. The STBM sleeves contain two laminae: a thick, inner basal lamina that was formed in vivo between Sertoli cells and peritubular myoid cells; and a thinner, outer basal lamina that was formed between myoid cells and sinusoidal endothelial cells. Characterization by immunofluorescence and SDS PAGE revealed that the isolated STBM retained fibronectin, laminin, and putative type IV collagen among its many components. When the STBM sleeves were gently shaken with an enriched fraction of primary Sertoli cells, the Sertoli cells bound preferentially to the lumenal basal lamina at the ends of the STBM sleeves. Few Sertoli cells bound to either the outer basal lamina of the STBM sleeves or to vascular extracellular matrix material which contaminated the STBM preparation. 3T3 cells, in contrast, bound to all surfaces of the STBM sleeves. Pretreatment of the STBM sleeves with proteases, 0.1 M Na metaperiodate, 4 M guanidine HCl, or heating to 80 degrees-90 degrees C inhibited lumenal Sertoli cell binding, but binding was not inhibited by chondroitinase ABC, heparinase, hyaluronidase, or 4 M NaCl. The lumenal Sertoli cell binding occurred in the presence or absence of added soluble laminin, but not fibronectin. The addition of soluble laminin, but not fibronectin, restored random binding of Sertoli cells to trypsinized STBM sleeves. Our in vitro model system indicates that Sertoli cells recognize differences in two basal laminae produced in vivo on either side of myoid cells.

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Page, Kathleen Creed, Paul B. Mason, Lynn Lindstrom, James S. Swan, and Sally E. Nyquist. "Dolichol and N-linked oligosaccharide synthesis in the rat testis: interaction between Sertoli and spermatogenic cells, evidence for paracrine effects." Biochemistry and Cell Biology 70, no. 6 (June 1, 1992): 496–503. http://dx.doi.org/10.1139/o92-077.

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The relative contribution of the Sertoli cell and the pachytene spermatocyte to dolichol and N-linked oligosaccharide biosynthesis within the seminiferous tubule was investigated. Evidence is presented to show that the interaction between these two cell types affects dolichol and N-linked oligosaccharide biosynthesis. Analysis of the dolichol content of Sertoli cultures confirms earlier data suggesting that the Sertoli cell constitutes the major pool of dolichols within the seminiferous tubule. [14C]Acetate incorporation studies suggest that the Sertoli cell in culture synthesizes dolichol much more rapidly than does the isolated pachytene spermatocyte. This information, in addition to previous data in the literature, infers an interactive effect whereby the presence of the spermatogenic cell in the tubule stimulates dolichol synthesis in the Sertoli cell. The absence of normal Sertoli-spermatocyte interactions in in vitro incubations may also limit dolichol synthesis in the pachytene spermatocyte. The distribution of dolichol kinase between the Sertoli and the pachytene spermatocyte was also examined. The concentration of this enzyme in the Sertoli cell suggests the presence of an active salvage pathway within that cell. The correlation between the appearance of the pachytene spermatocyte and the previously described peak of dolichol kinase activity in the seminiferous tubules of the prepubertal animal implies cell–cell interactions. Radiolabelling studies of N-linked oligosaccharides were conducted using [3H]mannose and concanavalin A affinity chromatography to identify multiantennary, biantennary, and high-mannose oligosaccharide pools. An in vitro bicameral coculture system was used to demonstrate that pachytene spermatocytes stimulate incorporation of [3H]mannose into Sertoli cell oligosaccharides. The presence of spermatocytes also induced a shift of label from the multiantennary oligosaccharide pool to the high-mannose pool in the Sertoli cell. Reciprocal experiments, in which the pachytene spermatocyte oligosaccharide pools were observed, showed no significant changes. These studies show a clear pachytene spermatocyte derived paracrine effect on Sertoli cell glycosylation.Key words: glycoprotein, dolichol, Sertoli, spermatocyte.

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Palmero, S., M. Prati, F. Bolla, and E. Fugassa. "Tri-iodothyronine directly affects rat Sertoli cell proliferation and differentiation." Journal of Endocrinology 145, no. 2 (May 1995): 355–62. http://dx.doi.org/10.1677/joe.0.1450355.

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Abstract The addition of physiological concentrations (1 nm) of tri-iodothyronine (T3) to the culture medium of Sertoli cells from prepubertal (8-day-old) rats stimulated both protein synthesis (+55%) and lactate (+50%) production, while it inhibited DNA synthesis (−30/35%) and aromatase activity (−45/50%); insignificant T3-dependent effects were observed in cultured Sertoli cells from midpubertal (28-day-old) rats. These data suggest an age-dependent role for thyroid hormone in promoting and maintaining Sertoli cell differentiation at puberty; moreover, the hormone is involved in the regulation of Sertoli cell proliferation. The present study validates the role of Sertoli cells as a specific target for T3 action at the testis level; it also demonstrates the existence of an early and critical direct influence of thyroid hormone on Sertoli cell proliferation and functional maturation. Journal of Endocrinology (1995) 145, 355–362

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Chuang, Chin-kai, Kun-Hsiung Lee, Chio-Tin Fan, and Yu-Show Su. "FSH-Sensitive Murine Sertoli Cell Lines Immortalized by Human Telomerase Gene hTERT Express the Androgen Receptor in Response to TNF-α Stimulation." Bioscience Reports 27, no. 6 (November 20, 2007): 403–11. http://dx.doi.org/10.1007/s10540-007-9063-y.

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Sertoli cells are regulated by follicular stimulating hormone (FSH) and testosterone secreted by the pituitary gland and Leydig cells, respectively. However, the expression of the FSH receptor and androgen receptor were undetectable in both primary cultured Sertoli cells and Sertoli cell lines immortalized by SV40 large T antigen. Two Sertoli cell lines, B6Sc-2 and B6Sc-3, were established from the testis of 19-day-old C57BL/6 mice testis by immortalization with human telomere reverse transcriptase. These Sertoli cell lines expressed FSH receptors and the total phosphoprotein patterns were converted after FSH treatment. Additionally, immunological methods demonstrated that these cell lines expressed characteristic Sertoli cell proteins, such as tyrosine-tubulin, vimentin and stem cell factor (SCF). Reverse transcription-polymerase chain reaction (RT-PCR) also indicates that they express Sertoli specific mRNAs, such as Amh, claudin11 and ZO-1. The expression of the androgen receptor in both B6Sc-2 and B6Sc-3 cells could be induced by TNF-α treatment. The present results indicate that these Sertoli cell lines are more native than others and may thus provide useful tools for in vitro studies.

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Golat, Brian T., and Don F. Cameron. "Sertoli Cells Enhance Formation of Capillary-Like Structures in Vitro." Cell Transplantation 17, no. 10-11 (October 2008): 1135–44. http://dx.doi.org/10.3727/096368908787236512.

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Sertoli cells isolated from the testis (referred to as extratesticular Sertoli cells) have been shown to facilitate allo- and xenogeneic cell transplantations. It appears likely that the ability of these cells to enhance the success of cell engraftment is due, in part, to the retention of their intratesticular functions of trophic support and immunoprotection. Sertoli cells also are involved in the regulation of angiogenesis in the testis, which may also contribute to enhanced cell engraftment success facilitated by extratesticular Sertoli cells. Because the maintenance of the cell's intratesticular angiogenic function has not yet been evaluated for extratesticular Sertoli cells, this study examined the cell's ability to enhance angiogenesis in vitro. Sertoli cell conditioned media were derived from isolated rat Sertoli cell cultures and used in a rat aortic model of induced angiogenesis, in endothelial and smooth muscle cell monocultures, and in endothelial smooth muscle cocultures. An angiogenic rat cytokine array identified angiogenic factors in the control and conditioned media. Aorta sections incubated with Sertoli cell conditioned media showed a marked increase in the formation of capillary-like structures when compared to controls. Likewise, endothelial cells incubated in conditioned media organized into capillary-like structures not observed when incubated in control media. In coculture, smooth muscle cells were associated with endothelial cell-derived capillary-like structures only when incubated in conditioned media. Cytokine arrays indicated the presence and a qualitative increase of specific angiogenic growth factors in Sertoli cell conditioned media not observed in control media. Results indicate that extratesticular Sertoli cells retain their intratesticular angiogenic function in vitro.

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