Testicular gonadotrophins and their receptors in human cryptorchidism as revealed by immunohistochemistry and radioreceptor assay

1986 ◽  
Vol 111 (1) ◽  
pp. 128-132 ◽  
Author(s):  
Outi Hovatta ◽  
I. Huhtaniemi ◽  
T. Wahlström
Keyword(s):  
Sertoli Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Radioreceptor Assay ◽  
Human Testis ◽  
Immunoperoxidase Technique ◽  
Fsh Receptor ◽  
Lh Receptor ◽  
And Control ◽  
Testicular Macrophages

Abstract. The localisation of endogenous FSH and LH was studied in 4 inguinal adult human testes by the immunoperoxidase technique utilising antisera against the β-subunits of human FSH and LH. The content of available FSH and LH receptors was determined by radioreceptor assay. The Sertoli cells and about 10% of cells in the intersitium the Leydig cells, possibly the testicular macrophages, were similarly FSH-positive in cryptorchidism and control testes. The FSH receptor levels per testis were significantly lower in cryptorchidism than in control testes. Also the localisation of LH in Leydig cells in cryptorchidism was similar to the control testes, but the LH receptor level was significantly lower. These data bring further evidence for Leydig and Sertoli cell malfunction in the inguinal human testis.

scholarly journals Exogenous Gonadotrophin Stimulation Induces Partial Maturation of Human Sertoli Cells in a Testicular Xenotransplantation Model for Fertility Preservation

2020 ◽  
Vol 9 (1) ◽  
pp. 266 ◽  
Author(s):  
Marsida Hutka ◽  
Lee B. Smith ◽  
Ellen Goossens ◽  
W. Hamish B. Wallace ◽  
Jan-Bernd Stukenborg ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Sertoli Cells ◽  
Connexin 43 ◽  
Xenograft Model ◽  
Cell Maturation ◽  
Human Testis ◽  
Testicular Development ◽  
Future Fertility ◽  
And Function ◽  
Testis Tissue

The future fertility of prepubertal boys with cancer may be irreversibly compromised by chemotherapy and/or radiotherapy. Successful spermatogenesis has not been achieved following the xenotransplantation of prepubertal human testis tissue, which is likely due to the failure of somatic cell maturation and function. We used a validated xenograft model to identify the factors required for Leydig and Sertoli cell development and function in immature human testis. Importantly, we compared the maturation status of Sertoli cells in xenografts with that of human testis tissues (n = 9, 1 year-adult). Human fetal testis (n = 6; 14–21 gestational weeks) tissue, which models many aspects of prepubertal testicular development, was transplanted subcutaneously into castrated immunocompromised mice for ~12 months. The mice received exogenous human chorionic gonadotropin (hCG; 20IU, 3×/week). In xenografts exposed continuously to hCG, we demonstrate the maintenance of Leydig cell steroidogenesis, the acquisition of features of Sertoli cell maturation (androgen receptor, lumen development), and the formation of the blood–testis barrier (connexin 43), none of which were present prior to the transplantation or in xenografts in which hCG was withdrawn after 7 months. These studies provide evidence that hCG plays a role in Sertoli cell maturation, which is relevant for future investigations, helping them generate functional gametes from immature testis tissue for clinical application.

Studies on primate gonadotropin receptors: comparison of follitropin and lutropin receptors in human testis

1983 ◽  
Vol 61 (7) ◽  
pp. 561-568 ◽  
Author(s):  
M. I. Berman ◽  
M. R. Sairam
Keyword(s):  
Dissociation Constants ◽  
Specific Binding ◽  
Particulate Fraction ◽  
Human Testis ◽  
Fsh Receptor ◽  
Lh Receptor ◽  
Adult Men ◽  
Human Choriogonadotropin ◽  
Marked Preference ◽  
Old Men

The interaction of 125I-labeled human follitropin (hFSH), human lutropin (hLH), and human choriogonadotropin (hCG) with a particulate fraction prepared from the testes of adult men was investigated. The hormone specific binding was maximal at pH 7.5 and 34 °C in the presence of 10 mM MgCl2. The FSH receptor was relatively more stable than the LH receptor (t1/2 at 34 °C of 14 and 4 h, respectively). The dissociation constants (Kd) calculated for hLH or hCG were very similar (approximately 1.0 × 10−10 – 1.4 × 10−10 M). The affinity of FSH and LH to their receptors did not appear to change with age, as shown from analysis of testes from 17- to 80-year-old men. The number of FSH receptors was greater than the number of LH receptors in these tissues. The hFSH receptor did not show any preference to binding of the homologous hormone, because FSH from nonprimates could displace 125I-labeled hFSH, but the LH receptor showed a marked preference for hLH or hCG as the ligand.

Immunocytochemical localization of hFSH as an index of Sertoli cell function in the human testis

1987 ◽  
Vol 116 (3) ◽  
pp. 333-338 ◽  
Author(s):  
Doug J. Yoon ◽  
Mircea Golimbu ◽  
Roger Schinella ◽  
Bruce Stein ◽  
Charles A. Sklar ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Seminiferous Tubule ◽  
Cell Function ◽  
Basal Membrane ◽  
Testicular Tissue ◽  
Human Testis ◽  
Immunoperoxidase Technique ◽  
Immunocytochemical Localization ◽  
Specific Staining

Abstract. The FSH receptor in the human testis has not been well characterized in vivo. Using an immunoperoxidase technique we have attempted the immunocytochemical localization of FSH in testicular tissue from patients with a variety of disorders including oligo- or azoospermia (N = 6), cryptorchidism (N = 3), and prostatic carcinoma (N = 3). Specific staining for hFSH was observed inside the seminiferous tubule, generally near the basal membrane in all except the cryptorchid patients. Specific staining was also localized in the luminal area of the seminiferous tubule. In most cases, FSH-positive cells were also found in the interstitium, with a minority of the cells being macrophages. The latter were more prevalent in the undescended testes and in orchiectomy specimens from patients with prostatic cancer. The pattern of FSH localization observed in this study probably represents receptorbound hormone, and may reflect damage to the Sertoli cell and its tight junctions. Further study of the changes in receptor distribution as an indication of Sertoli cell malfunction, may be helpful in our understanding of human testicular disorders.

Adult rat Sertoli cells secrete a factor or factors which modulate Leydig cell function

1987 ◽  
Vol 114 (3) ◽  
pp. 459-467 ◽  
Author(s):  
V. Papadopoulos ◽  
P. Kamtchouing ◽  
M. A. Drosdowsky ◽  
M. T. Hochereau de Reviers ◽  
S. Carreau
Keyword(s):  
Cyclic Amp ◽  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Interaction ◽  
Adult Rats ◽  
Adult Rat ◽  
Stimulating Factor

ABSTRACT Production of testosterone and oestradiol-17β by Leydig cells from adult rats was stimulated by LH or dibutyryl cyclic AMP (10 and 2·5-fold respectively). The addition of spent medium from normal, hemicastrated or γ-irradiated rat seminiferous tubule cultures, as well as from Sertoli cell cultures, to purified Leydig cells further enhanced both basal (44 and 53% for testosterone and oestradiol-17β respectively) and LH-stimulated (56 and 18%) steroid output. Simultaneously, a decrease (20–30%) in intracellular cyclic AMP levels was observed. This stimulating factor (or factors) secreted by the Sertoli cells is different from LHRH, is of proteinic nature and has a molecular weight ranging between 10 000 and 50 000; its synthesis is not controlled by FSH nor by testosterone. This factor(s) involved in rat Leydig cell steroidogenesis, at a step beyond the adenylate cyclase, does not require protein synthesis for testosterone formation whereas it does for oestradiol-17β production. It should be noted that a germ cell–Sertoli cell interaction modulates the synthesis of this factor(s). J. Endocr. (1987) 114, 459–467

scholarly journals THE EFFECT OF CHRONIC EXPOSURE OF NICOTINE INHALATION TO THE COUNT OF SPERMATOGONIA, SERTOLI CELLS AND LEYDIG CELLS OF YOUNG WHITE RAT WISTAR STRAIN

2019 ◽  
Vol 26 (2) ◽  
Author(s):  
Aril Rizaldi ◽  
Doddy M Soebadi ◽  
Soetojo Soetojo
Keyword(s):  
Cell Count ◽  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Chronic Exposure ◽  
Leydig Cells ◽  
Control Group ◽  
Nicotine Exposure ◽  
Control Group Design ◽  
Wistar Strain

Objective: To analyze the difference in the number of spermatogonia, leydig cells and sertoli cells in young age of  white mice Wistar strain after inhalation of chronic nicotine exposure. Material & Method: Laboratory experimental study with post test only control group design, measurement of spermatogonium, leydig cell, sertoli cell in 5 groups of young male Wistar strain, negative control group and treatment group given nicotine exposure 0.5 mg, 1 mg, 2 mg, and 4 mg/kg body weight/day for 30 days. Results: A significant reduction in spermatogonium was found in the group given nicotine 0.5 mg/kgBW/day (p=0.048), 1 mg/kgBW/day (p=0.002), 2 mg/kgBW/day (p=0.002) and 4 mg/kgBW/day (p=0.000) when compared to the control group. Significant decreases were also seen in the group receiving 4 mg of nicotine exposure compared with 0.5 mg (p=0.018). Significant decrease in sertoli cell count was seen only in the nicotine group of 4 mg/kgBW/day compared with the control group (p=0.047). A significant decrease in leydig cell count was found in the nicotine 2 mg/kgBW/day (p=0.037) and nicotine group 4 mg/kgBW/day (p=0.023) when compared with the control group. Significant decreases were also found in the 4 mg/kgBW/day group compared to the 0.5 mg/kgBW/day group (p=0.004). In this study there were also a decrease in the number of spermatogonia, sertoli cells, and leydig cells in the increased dose of nicotine given although not statistically significant. Conclusion: Chronic exposure of nicotine per inhalation may decrease the number of spermatogonia, sertoli cells, and leydig cells. The higher the dose of nicotine given the greater the decrease in the number of spermatogonium cells, sertoli cells, and leydig cells that occur. This proves that nicotine is one of the causes of infertility in men.

scholarly journals Androgen Receptor Distribution in Adult Human Testis1

1999 ◽  
Vol 84 (1) ◽  
pp. 350-358 ◽  
Author(s):  
Carlos A. Suárez-Quian ◽  
Francisco Martínez-García ◽  
Manuel Nistal ◽  
Javier Regadera
Keyword(s):  
Androgen Receptor ◽  
Sertoli Cell ◽  
Leydig Cells ◽  
Staining Intensity ◽  
Seminiferous Epithelium ◽  
Stage Iii ◽  
Human Testis ◽  
Immunoperoxidase Method ◽  
Myoid Cells ◽  
Cell Nuclei

The distribution of the androgen receptor (AR) in archival human testes was determined immunocytochemically using an affinity-purified peptide-specific rabbit antibody, PG21, and employing a modified biotin-streptavidin-immunoperoxidase method that incorporated a biotin amplification step. In combination with microwave epitope retrieval, the biotin amplification step increased the sensitivity of the immunostaining assay approximately 20-fold. Thus, the useful range at which PG21 rendered a robust, specific immunostaining signal without also increasing nonspecific background was extended dramatically. Broadening the useful range of the PG21 antibody made it possible to resolve the relative amounts of immunopositive AR in different cell types of the human testis. At a high PG21 concentration, for example, all AR-positive cells exhibited a robust immunostaining intensity, but it was not possible to distinguish between nuclei exhibiting either high or moderate immunostaining intensities. In contrast, as the concentration of PG21 was decreased, distinct populations of testicular cells exhibited differential AR immunostaining intensities in their nuclei. AR immunostaining of Sertoli cell nuclei was present at low PG21 concentrations at which no immunostaining of peritubular myoid cells or Leydig cells could be detected. In turn, AR immunostaining of peritubular myoid cells was detected at PG21 concentrations that did not immunostain Leydig cells. Moreover, within the seminiferous epithelium, Sertoli cell nuclear AR staining intensity was less at stages V and VI of the cycle of the seminiferous epithelium than that at stage III, and stage III staining intensity was greater than that at stages I and II. This AR immunostaining pattern in human Sertoli cell nuclei as a function of the cycle of the seminiferous epithelium is reminiscent of the pattern observed in rodent species. Finally, no AR immunostaining of germ cells was observed at any of the PG21 concentrations examined.

scholarly journals Use of antibodies against LH receptor, 3beta-hydroxysteroid dehydrogenase and vimentin to characterize different types of testicular tumour in dogs

Reproduction ◽  
2001 ◽  
pp. 287-296 ◽  
Author(s):  
MA Peters ◽  
KJ Teerds ◽  
I van der Gaag ◽  
DG de Rooij ◽  
FJ van Sluijs
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Hydroxysteroid Dehydrogenase ◽  
Histological Diagnosis ◽  
Lh Receptor ◽  
Testicular Tumours ◽  
Sertoli Cell Tumours ◽  
Mixed Tumours ◽  
Leydig Cell Tumours

Testicular tumours in dogs are of Sertoli cell, Leydig cell or germinal origin and mixed tumours are also frequently observed. The cellular components of mixed tumours are usually identified by histological examination but sometimes this is difficult. In this study, a panel of specific antibodies was used to identify the different cell types in testicular tumours by immunohistochemistry. Leydig cells were identified using an antibody against the LH receptor and an antibody against the steroidogenic enzyme 3beta-hydroxysteroid dehydrogenase (3beta-HSD), both of which are characteristic of Leydig cells in testes. Sertoli cells were identified using an antibody against the intermediate filament vimentin. Seminoma cells did not stain with any of these antibodies. Vimentin was used only in histologically complex cases. Eighty-six tumours, diagnosed histologically as 29 Sertoli cell tumours, 25 Leydig cell tumours, 19 seminomas and 13 mixed tumours, were studied. Feminization was observed in 17 dogs. Leydig cell tumours stained positively with the antibodies against the LH receptor and 3beta-HSD, whereas seminomas and Sertoli cell tumours were negative (unstained). The antibody against vimentin stained both Sertoli and Leydig cells, and tumours arising from these cells, but not seminomas. Immunohistochemistry revealed that three tumours identified histologically as Sertoli cell tumours were actually Leydig cell tumours. In 14 dogs the histological diagnosis appeared to be incomplete, as mixed tumours instead of pure types of tumours were identified in 11 dogs, and in three dogs mixed tumours appeared to be pure types. Hence, the histological diagnosis was insufficient in approximately 20% of dogs. Furthermore, immunohistochemical analysis of testis tumours revealed that feminization occurred in dogs with Sertoli cell tumours or Leydig cell tumours and their combinations, but not in dogs with a seminoma. In conclusion, incubation with antibodies against LH receptor and 3beta-HSD proved to be a consistently reliable method for identification of Leydig cell tumours in dogs. Vimentin can be used to discriminate between Sertoli cell tumours and seminomas. Overall, this panel of antibodies can be very useful for determination of the identity of testicular tumours in which histological characterization is complicated and the pathogenesis of feminization is not clear.

101. THE RELATIONSHIP BETWEEN SERTOLI CELL STATUS AND IDIOPATHIC MALE INFERTILITY

2010 ◽  
Vol 22 (9) ◽  
pp. 19
Author(s):  
J. T. Haverfield ◽  
P. G. Stanton ◽  
S. J. Meachem
Keyword(s):  
Tight Junctions ◽  
Sertoli Cell ◽  
Cell Population ◽  
Sertoli Cells ◽  
Testicular Biopsy ◽  
Human Testis ◽  
Testicular Function ◽  
The Status ◽  
The Relationship ◽  
Infertile Patients

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.

Immunodetection of inhibin in the human testis and epididymis during normal development and in non-tumoural testicular lesions

2010 ◽  
Vol 22 (3) ◽  
pp. 558 ◽  
Author(s):  
Manuel Nistal ◽  
Pilar González-Peramato ◽  
Maria P. De Miguel
Keyword(s):  
Sertoli Cells ◽  
Leydig Cells ◽  
Staining Pattern ◽  
Hormonal Treatment ◽  
Human Testis ◽  
Seminiferous Tubules ◽  
Secretory Cells ◽  
Testicular Function ◽  
Human Epididymis ◽  
Efferent Ducts

Plasma concentrations of inhibin are correlated with spermatogenetic function. Inhibin is secreted mainly by the Sertoli and Leydig cells of the testis. In the human epididymis, the location and function of inhibin are contentious. Thus, the aim of the present study was to determine the location of inhibin in the human epididymis. Investigations were performed in samples with normal testicular function at different stages of development, as well as in samples in which testicular function or the testicular–epididymal connection were altered. In fetal, newborn and infant testes, Sertoli and Leydig cells stained positive for inhibin, whereas no such staining was detected in the epididymides. Inhibin was located in both the Sertoli and Leydig cells, as well as in the epididymis, in the apical pole of mainly secretory cells in the efferent ducts. This staining pattern was not correlated with the staining pattern for macrophages. The main duct of the epididymis was negative for inhibin staining. In ischaemic atrophic testes, the few tubules in which Sertoli cells were present stained positive for inhibin, whereas the epididymides stained negative. In paediatric cryptorchidism, Sertoli and Leydig cells stained positive for inhibin, whereas the epididymides were negative. In adult cryptorchidism, Sertoli and Leydig cells stained positive for inhibin, even in tubules containing Sertoli cells only. Interestingly, inhibin was absent from the efferent ducts. In three cases undergoing hormonal treatment prior to subsequent gender change, Sertoli and Leydig cells stained positive for inhibin. In contrast, the efferent ducts were negative or only faintly positive in cases of shorter hormonal treatment. In all cases studied, the presence of inhibin in the efferent ducts was associated with its production in the testis, suggesting that the epididymis is not responsible for the production of inhibin in men. The pattern of inhibin staining does not correlate with that of macrophages, suggesting that inhibin is not degraded in the human epididymis. The data suggest that, in humans, inhibin is secreted by Sertoli cells into the seminiferous tubules and then travels towards the efferent ducts, where it is reabsorbed into the bloodstream.

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