Expression of the glucocorticoid receptor and 11β-hydroxysteroid dehydrogenase 2 in pig testes cells along fetal development

2007 ◽  
Vol 19 (5) ◽  
pp. 664 ◽  
Author(s):  
S. Haeussler ◽  
R. Claus
Keyword(s):  
Germ Cells ◽  
Leydig Cell ◽  
Fetal Development ◽  
Leydig Cells ◽  
Cell Function ◽  
Hydroxysteroid Dehydrogenase ◽  
Immunocytochemical Staining ◽  
Tunel Staining ◽  
Steroid Synthesis ◽  
Leydig Cell Function

The glucocorticoid (GC)–cortisol receptor (GCR)–11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) system is involved in the regulation of Leydig cell function and spermatogenesis in mature animals. Herein, we describe the expression of the GCR and 11β-HSD2 and the occurrence of apoptosis during fetal development. Male fetuses were collected from Weeks 6, 10, 13, and 15 of pregnancy and from neonates. The testes were used for the immunocytochemical staining of GCR, 11β-HSD2 and for terminal deoxyribonucleotidyl transferase-mediated dUTP–digoxigenin nick end-labelling (TUNEL) staining of apoptosis. Apoptosis did not occur in any Leydig cells, but approximately 30% expressed GCR and 11β-HSD2. The number of GCR-positive cells was similar at all stages, but the number of 11β-HSD2-positive cells tended to be higher at Weeks 6 and 15. Steroid synthesis was also higher compared with Weeks 10 and 13. Apoptosis occurred in only a few germ cells. Nearly all germ cells were GCR positive at Weeks 10 and 13, when 11β-HSD2 was also increased. The total number of 11β-HSD2-positive germ cells was approximately 30%. Thus, elevated GCR expression coincided with the differentiation of gonocytes to spermatogonia and their migration to the basal lamina.

Steroid metabolism by a tumour of the specific gonadal stroma in a child

1982 ◽  
Vol 99 (4) ◽  
pp. 624-629 ◽  
Author(s):  
Alicia Barmach de Niepomniszcze ◽  
Marco A. Rivarola ◽  
Héctor E. Chemes ◽  
César Bergadá
Keyword(s):  
Leydig Cell ◽  
Sertoli Cells ◽  
Sexual Development ◽  
Cell Function ◽  
Hydroxysteroid Dehydrogenase ◽  
Steroid Metabolism ◽  
Male Pseudohermaphroditism ◽  
Testosterone Biosynthesis ◽  
Pubertal Boys ◽  
Leydig Cell Function

Abstract. A study of steroid metabolism by a tumour of the specific gonadal stroma was carried out in a 10 year old boy. Tumours developed in the two testes from multiple foci, and clinically, no signs of sexual development were evident. Four testicular enzymes necessary for testosterone biosynthesis were estimated in the child, in two adult controls, and in three pre-pubertal boys with male pseudohermaphroditism but normal tests of Leydig cell function. 17α-Hydroxylase and 17β-hydroxysteroid dehydrogenase were similar in the five controls and in the gonad with the tumour, while 17,20-desmolase and 3β-hydroxysteroid dehydrogenase were grossly deficient in the child with the tumour. These enzyme deficiencies might explain the absence of peripheral virilization in a boy with a tumour of Leydig and Sertoli cells.

INSL3: A Marker of Leydig Cell Function and Testis-Bone-Skeletal Muscle Network

2020 ◽  
Vol 27 (12) ◽  
pp. 1246-1252
Author(s):  
Paolo Facondo ◽  
Andrea Delbarba ◽  
Filippo Maffezzoni ◽  
Carlo Cappelli ◽  
Alberto Ferlin
Keyword(s):  
Skeletal Muscle ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Damage ◽  
Endocrine Function ◽  
Testicular Descent ◽  
Male Hypogonadism ◽  
Adult Men ◽  
Leydig Cell Function

This article reviews the role of INSL3 as biomarker of Leydig cell function and its systemic action in testis-bone-skeletal muscle crosstalk in adult men. Insulin-like factor 3 (INSL3) is a peptide hormone secreted constitutively in a differentiation-dependent mode by testicular Leydig cells. Besides the role for the testicular descent, this hormone has endocrine anabolic functions on the bone-skeletal muscle unit. INSL3 levels are low in many conditions of undifferentiated or altered Leydig cell status, however the potential clinical utility of INSL3 measurement is not yet well defined. INSL3 levels are modulated by the long-term cytotropic effect of the hypothalamicpituitary- gonadal axis, unlike testosterone that is acutely sensitive to the stimulus by luteinizing hormone (LH). INSL3 directly depends on the number and differentiation state of Leydig cells and therefore it represents the ideal marker of Leydig cell function. This hormone is more sensitive than testosterone to Leydig cell impairment, and the reduction of INSL3 in adult men can precociously detect an endocrine testicular dysfunction. Low INSL3 levels could cause or contribute to some symptoms and signs of male hypogonadism, above all sarcopenia and osteoporosis. The measurement provided suggested that the measurement of INSL3 levels should be considered in the clinical management of male hypogonadism and in the evaluation of testicular endocrine function. The monitoring of INSL3 levels could allow an early detection of Leydig cell damage, even when testosterone levels are still in the normal range.

scholarly journals Autoradiographical Localization of Luteinizing Hormone Releasing Hormone (LHRH) Receptors on Rat Testicular Intertubular Cells Fractionated on Percoll Density Gradients

1985 ◽  
Vol 38 (4) ◽  
pp. 435 ◽  
Author(s):  
MP Hedger ◽  
OP Risbridger ◽  
DM de Kretser
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Specific Binding ◽  
Density Gradients ◽  
Direct Stimulation ◽  
Density Region ◽  
Luteinizing Hormone Releasing Hormone ◽  
Testicular Cells ◽  
Leydig Cell Function

The specific binding of 125I-1abelled [D-Ser(tBu)6,des-GlyNH21OJ LHRH ethylamide (LHRH-A) to testicular intertubular cells fractionated on Percoll density gradients was investigated. The greatest binding per cell occurred in the density region which contained the largest proportion of Leydig cells (sp. gr. 1�0820-1�0585). Autoradiographs of the cells from this region confirmed that silver stains were predominantly located over the Leydig cell, significantly (P < 0�01) more grains were observed over this cell type in the total binding fractions than in the non-specific binding fractions. However, 5�9% of cells other than Leydig cells (testicular macrophages and indeterminate connective tissue cells) from this region also displayed significant disp1aceable binding (P < 0�01). The location of HRH-A binding to cells in other density regions, which did not contain identifiable Leydig cells, could not be established by autoradiography. These results confirm that the Leydig cell possesses LHRH receptors, but also indicate that other testicular cells have specific, highaffinity binding sites for LHRH-A, and may either be responsive to direct stimulation by LHRH, or may partially mediate the effects of LHRH and its agonists on Leydig cell function.

CHANGES IN LEYDIG CELL HYDROXYSTEROID DEHYDROGENASES INDUCED BY ADMINISTRATION OF TESTOSTERONE PROPIONATE TO NORMAL MEN

1974 ◽  
Vol 60 (1) ◽  
pp. 175-NP ◽  
Author(s):  
H. C. MORSE ◽  
C. G. HELLER
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Testosterone Propionate ◽  
Testicular Biopsy ◽  
Frozen Sections ◽  
Histochemical Technique ◽  
Biopsy Specimens ◽  
Normal Men ◽  
Leydig Cell Function

SUMMARY By the employment of an improved histochemical technique, frozen sections from human testicular biopsy specimens were examined for 3β-and 17β-hydroxysteroid dehydrogenase (HSD) activity, before, during, and after administration of 25 or 50 mg testosterone propionate per day to normal men. This administration strongly suppressed Leydig cell HSD activity and caused these cells to be transformed into fibroblast-like cells. After cessation of administration, the Leydig cells recovered morphologically and so did, simultaneously their 3β- and 17β-HSD activity. It is concluded that histochemically detectable 3β- and 17β-HSD are under gonadotrophin control and change with alterations in Leydig cell function. The morphology or 3β- and 17β-HSD are therefore probably acceptable as indicators of Leydig cell function in reproductively normal men.

scholarly journals Impaired Leydig Cell Function in Infertile Men: A Study of 357 Idiopathic Infertile Men and 318 Proven Fertile Controls

2004 ◽  
Vol 89 (7) ◽  
pp. 3161-3167 ◽  
Author(s):  
A.-M. Andersson ◽  
N. Jørgensen ◽  
L. Frydelund-Larsen ◽  
E. Rajpert-De Meyts ◽  
N. E. Skakkebæk
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Infant Development ◽  
Cell Function ◽  
Serum Testosterone ◽  
Seminiferous Epithelium ◽  
Lower Serum ◽  
Infertile Men ◽  
Serum Lh ◽  
Leydig Cell Function

Abstract To investigate whether an impaired Leydig cell function is present in severely oligospermic men, serum testosterone (T), LH, estradiol (E2), and SHBG levels in 357 idiopathic infertile men were compared with levels in 318 proven fertile men. In addition, the T/LH ratio, E2/T ratio, and calculated free T index (cFT) were compared between the two groups. A shift toward lower serum T levels, cFT, and T/LH ratio and higher serum LH, E2, and E2/T levels was observed in the group of infertile men. On average, the infertile men had 18, 26, and 34% lower serum T, cFT, and T/LH levels, respectively, and 19, 18, and 33% higher serum LH, E2, and E2/T levels, respectively, than the fertile men. Twelve percent of the infertile men had a serum T level that fell below the 2.5 percentile of the fertile levels, and 15% of the infertile men had a LH level that was above the 97.5 percentile of the fertile levels. Thus, the group of infertile men showed significant signs of impaired Leydig cell function in parallel to their impaired spermatogenesis. The association of decreased spermatogenesis and impaired Leydig cell function might reflect a disturbed paracrine communication between the seminiferous epithelium and the Leydig cells, triggered by distorted function of the seminiferous epithelium. On the other hand, the parallel impairment of spermatogenesis and Leydig cells may reflect a congenital dysfunction of both compartments caused by a testicular dysgenesis during fetal/infant development.

THE MECHANISMS INVOLVED IN TESTICULAR DEGENERATION IN MAN

1967 ◽  
Vol 56 (4_Suppl) ◽  
pp. S17-S40 ◽  
Author(s):  
Svend G. Johnsen
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Frequent Occurrence ◽  
Human Testis ◽  
Cell Hyperplasia ◽  
Number Of Factors ◽  
Leydig Cell Hyperplasia ◽  
Leydig Cell Function ◽  
Testicular Degeneration

ABSTRACT The study presents a correlation between the regulatory mechanisms of the human testis and a number of factors involved in the degenerative processes in idiopathic hypospermatogenesis. As a working hypothesis, it is assumed that temporary damage cannot result in permanent hypospermatogenesis unless this is maintained by a special mechanism, and the object of the study is to find such a mechanism. It is shown 1) that in man the full spermatogenetic cycle can take place in the absence of Leydig cells; 2) that decreased spermatogenesis leads to increased release of gonadotrophins and further to Leydig cell hyperplasia; 3) that spermatogenetic lesions do not per se induce deposition of hyaline material in the tubular wall, but that hyalinization damages the epithelium; 4) that a special feature of the structure of the testis in Klinefelter's syndrome strongly suggests that the hyalinization process is not a direct gonadotrophin effect but is related to Leydig cell function. The nature of Leydig cell function has been shown to depend upon the qualitative nature of gonadotrophin stimulation, and findings indicating a qualitative change in the secretion of hyperplastic Leydig cells in hypospermatogenesis are presented. From these relationships a theory of the pathogenesis of "idiopathic" hypospermatogenesis is advanced. Temporary damage to the germinal epithelium induces increased gonadotrophin release and changes in the FSH/LH ratio. These result in Leydig cell hyperplasia and in qualitative changes in Leydig cell function. This may start a hyalinization process which damages the epithelium, this damage in turn maintains the gonadotrophin rise, etc., etc., The existence of a pathogenetic vicious circle in the human testis affords an explanation for the frequent occurrence of testicular degeneration and permanent cryptogenetic, hypospermatogenesis in man. The aim of this presentation is to correlate the mechanisms involved in the regulation of testicular function in man with the processes of non-specific testicular degeneration. By a total consideration of a large number of factors an attempt will be made to arrive at an explanation of the frequent occurrence of testicular degeneration in man. Although testicular degeneration has frequently been dealt with in the literature (cf. below), no such attempt has apparently been published.

scholarly journals Androgen and Luteinizing Hormone Stimulate the Function of Rat Immature Leydig Cells Through Different Transcription Signals

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaoheng Li ◽  
Qiqi Zhu ◽  
Zina Wen ◽  
Kaimin Yuan ◽  
Zhijian Su ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Luteinizing Hormone ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Transcription Signals ◽  
Leydig Cell Function

The function of immature Leydig cells is regulated by hormones, such as androgen and luteinizing hormone (LH). However, the regulation of this process is still unclear. The objective of this study was to determine whether luteinizing hormone (LH) or androgens contribute to this process. Immature Leydig cells were purified from 35-day-old male Sprague Dawley rats and cultured with LH (1 ng/ml) or androgen (7α-methyl-19- nortestosterone, MENT, 100 nM) for 2 days. LH or MENT treatment significantly increased the androgens produced by immature Leydig cells in rats. Microarray and qPCR and enzymatic tests showed that LH up-regulated the expression of Scarb1, Cyp11a1, Cyp17a1, and Srd5a1 while down-regulated the expression of Sult2a1 and Akr1c14. On the contrary, the expression of Cyp17a1 was up-regulated by MENT. LH and MENT regulate Leydig cell function through different sets of transcription factors. We conclude that LH and androgens participate in the regulation of rat immature Leydig cell function through different transcriptional pathways.

Cultured Sertoli cell-mediated FSH stimulatory effect on Leydig cell steroidogenesis

1985 ◽  
Vol 248 (2) ◽  
pp. E176-E181
Author(s):  
M. Benahmed ◽  
J. Reventos ◽  
E. Tabone ◽  
J. M. Saez
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Activity ◽  
Defined Medium ◽  
Cell Number ◽  
Two Parameters ◽  
Leydig Cell Function

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.

Growth hormone-induced STAT5B regulates Star gene expression through a cooperation with cJUN in mouse MA-10 Leydig cells

Endocrinology ◽  
2021 ◽  
Author(s):  
Pierre-Olivier Hébert-Mercier ◽  
Francis Bergeron ◽  
Nicholas M Robert ◽  
Samir Mehanovic ◽  
Kenley Joule Pierre ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Mrna Levels ◽  
Leydig Cell Function ◽  
Star Gene

Abstract Leydig cells produce androgens that are essential for male sex differentiation and reproductive function. Leydig cell function is regulated by several hormones and signaling molecules, including growth hormone (GH). Although GH is known to upregulate Star gene expression in Leydig cells, its molecular mechanism of action remains unknown. The STAT5B transcription factor is a downstream effector of GH signaling in other systems. While STAT5B is present in both primary and Leydig cell lines, its function in these cells has yet to be ascertained. Here we report that treatment of MA-10 Leydig cells with GH or overexpression of STAT5B induces Star mRNA levels and increases steroid hormone output. The mouse Star promoter contains a consensus STAT5B element (TTCnnnGAA) at -756 bp to which STAT5B binds in vitro (EMSA and supershift) and in vivo (ChIP) in a GH-induced manner. In functional promoter assays, STAT5B was found to activate a -980 bp mouse Star reporter. Mutating the -756 bp element prevented STAT5B binding but did not abrogate STAT5B-responsiveness. STAT5B was found to functionally cooperate with DNA-bound cJUN. The STAT5B/cJUN cooperation was only observed in Leydig cells and not in Sertoli or fibroblast cells, indicating that additional Leydig cell-enriched transcription factors are required. The STAT5B/cJUN cooperation was lost only when both STAT5B and cJUN elements were mutated. In addition to identifying the Star gene as a novel target for STAT5B in Leydig cells, our data provide important new insights into the mechanism of GH and STAT5B action in the regulation of Leydig cell function.

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