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At least 145 records · Page 8Linked to original sources
PubMed1990

Short-term stimulatory effect of Sertoli cell conditioned medium on Leydig cell steroidogenesis is not mediated by inhibin.

Addition of concentrated rat Sertoli cell conditioned medium (rSCCM) to isolated Leydig cells from immature rats stimulated steroid production more than 13-fold within 4 h. LH-stimulated steroidogenesis was not enhanced by addition of rSCCM. The biological activity of the concentrated rSCCM was higher after incubation of Sertoli cells with FSH, whereas FSH alone did not stimulate steroid production. This effect of rSCCM was not due to inhibin, since highly purified 32 kDa rat inhibin, in doses equivalent to those present in rSCCM, had no effect on steroidogenesis during the 4 h incubation period. Furthermore, inhibin could be separated from the Leydig cell stimulating factor by anion-exchange chromatography. These results indicate a short-term paracrine control of Leydig cell steroidogenesis by Sertoli cell derived factors, which differ from inhibin.

Animals↗
PubMed1994

Adherence of lymphocytes to Leydig cell surface as an effect of the functional activity of Leydig cells in vitro.

Formation of lymphocyte rosettes around unstimulated and/or LH/hCG-treated Leydig cells in culture as well as in suspension was investigated. The ability of Leydig cells to interact with lymphocytes was positively correlated with their steroidogenic activity, as measured by means of a histochemical test for delta (5)3 beta-HSD activity and by radioimmunoassay for androgen level in culture media. In order to rule out nonspecific binding of lymphocytes, rosette specificity tests were performed. Time-dependent dynamics of cell-cell interaction was also followed. A phenomenon resembling phagocytosis of the adhered lymphocytes was observed after 4 h of co-culture. Morphology of this interaction was examined under light microscope and transmission electron microscope.

3-Hydroxysteroid Dehydrogenases↗
PubMed1987

Biological and biochemical characterization of estrogen-dependent mouse Leydig cell tumors.

Leydig cell tumors formed in BALB/c mice were found to be able to be transplanted subcutaneously in the same strain. One of the sublines, called T 22137, showed growth inhibition in response to estrogenization of host mice. The other subline (T 124958-O), which was originally classified as an estrogen-independent line, was observed to contain the low-affinity estradiol binding component in the cytosol fraction. At a later stage of transplantation, however, the growth of this subline was modestly but significantly enhanced by estrogenic stimuli. This alteration was accompanied by appearance of an estrogen receptor-like molecule which was associated with chromatin even in the absence of estrogen stimuli. In the presence of estrogen selection pressure, a new tumor line, designated as T 124958-R, was established, which showed marked estrogen-dependent growth. T 124958-R was found to contain the cytosolic estrogen receptor. The additional difference was that the annulate lamellae were identified only in T 124958-R, but not in T 124958, by electron microscopic studies. The estrogen dependency of T 124958-R was further substantiated by demonstration of an estrogen secretory protein as well as the estrogen-enhanced formation of 5 alpha-steroids. T 22137 showed growth inhibition in tamoxifen-treated mice. The growth of T 124958-R was enhanced by the administration of tamoxifen to mice. This tamoxifen-induced tumor growth was further stimulated by the simultaneous administration of estrogen. These observations would suggest that mouse Leydig cell tumor systems provide us with a valuable model to investigate the influence of estrogen as well as antiestrogen on malignant cells.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1995

Case report: congenital adrenal hyperplasia and malignant Leydig cell tumor.

Leydig cell tumors are very rarely seen testicular tumors and can be difficult to distinguish from testicular tumors of the adrenogenital syndrome. Testicular tumors of the adrenogenital syndrome are confined to patients with congenital adrenal hyperplasia. The authors report a case of a patient with malignant Leydig cell tumor and a history of congenital adrenal hyperplasia (adrenogenital syndrome). To the authors' knowledge, this has not been reported previously.

Adrenal Hyperplasia, Congenital↗
PubMed1995

Regulation of expression of steroidogenic enzymes in Leydig cells.

The Leydig cell of the testis is the only cell in the male that has the capacity to synthesize testosterone from cholesterol. Testosterone is critical during fetal development for male sexual differentiation, and postnatally for initiation and maintenance of spermatogenesis and the expression of the male secondary sex characteristics. The biosynthesis of testosterone requires the activities of four enzymes, cholesterol side-chain cleavage enzyme (P450scc), 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4 isomerase (3 beta HSD), 17 alpha-hydroxylase/C17-20 lyase (P450(17 alpha)), and 17-ketosteroid reductase. The expression of these enzymes appears to be regulated by different mechanisms. The recent isolation of the mouse cDNAs and structural genes that encode these enzymes has enabled us to begin to investigate the regulation of their expression at the molecular level. This review discusses the regulation by cAMP and steroids of three enzymes in Leydig cells, P450scc, P450(17 alpha), and 3 beta HSD, as well as characterization of the promoters of the mouse genes that encode P450scc and P450(17 alpha).

17-Hydroxysteroid Dehydrogenases↗
PubMed1994

Leydig cell heterogeneity as judged by quantitative cytochemistry of 3 beta-hydroxysteroid dehydrogenase activity in individual rat Leydig cells.

3 beta-Hydroxysteroid dehydrogenase (3 beta-HSD) is one of the key enzymes involved in the steroidogenic pathway of Leydig cells. In this study, quantitative cytochemistry was used to detect the 3 beta-HSD staining intensity in individual rat Leydig cells. The measurement of the intensity of staining was a reliable method reflecting the relative amount of 3 beta-HSD activity. The objective was to determine the presence, basal and hCG-mediated effect of 3 beta-HSD activity in individual Leydig cells. 3 beta-HSD cytochemistry was performed in both, 8 and 12 microns diameter rat Leydig cells. The results showed that both populations of Leydig cells have different basal 3 beta-HSD activity. The 8 microns cells showed a greater basal 3 beta-HSD activity than the 12 microns cells when their optical density values were normalized to their size. A difference in regulation of the enzymatic activity by LH/hCG was observed in the two types of Leydig cells. Incubation of the whole population of Leydig cells with hCG (1IU), decreased the 3 beta-HSD activity in the 8 microns cells, but increased the activity in the 12 microns cells. The results describe for the first time that the 3 beta-HSD activity may be differentially regulated by LH/hCG in Leydig cells.

3-Hydroxysteroid Dehydrogenases↗
PubMed1991

Pachytene spermatocytes regulate the secretion of Sertoli cell protein(s) which stimulate Leydig cell steroidogenesis.

The influence of germ cells (pachytene spermatocytes and round spermatids) on the secretion by Sertoli cells of the proteinaceous factor(s) which stimulates Leydig cell steroid biosynthesis was investigated. Sertoli cells from immature rats were cultured on plastic dishes or on Millipore filters impregnated with reconstituted basement membrane in bicameral chambers. Immature rat Sertoli cell secreted proteins (rSCSP; MW greater than 10,000), from conventional cultures, stimulated 4- to 5-fold steroid biosynthesis in normal rat and MA-10 mouse tumor Leydig cells, respectively. MA-10 cells were then used as a bioassay system for most studies, although purified rat Leydig cells were used in some cases to further confirm results obtained with MA-10 cells. rSCSP collected from both the apical and basal compartment of the chambers were examined for their ability to stimulate Leydig cell steroidogenesis. The Leydig cell stimulatory activity from Sertoli cells was found to be secreted in a polarized manner, with 80% of the total bioactivity found in the basal rSCSP. Addition of pachytene spermatocyte proteins (PSP) in the apical compartment of the chambers inhibited, in a time- and concentration-dependent manner, the basally directed Sertoli cell secretion of the Leydig cell stimulatory protein(s) by 85%. Similar results were obtained when freshly isolated pachytene spermatocytes were directly added on top of Sertoli cell epithelial sheets in the apical compartment of the chambers. In contrast, round spermatid proteins (RSP) did not exhibit a comparable effect to that of PSP in regulating the Sertoli cell secretion of the Leydig cell stimulatory activity. These results demonstrate that the Sertoli cell secreted protein(s) which stimulates Leydig cell steroid biosynthesis is secreted in a basally polarized direction, and its secretion is specifically modulated by pachytene spermatocytes.

Androgens↗
PubMed1998

Lactogenic hormone-inducible phosphorylation and gamma-activated site-binding activities of Stat5b in primary rat Leydig cells and MA-10 mouse Leydig tumor cells.

The signal transducer and activator of transcription Stat5b has been implicated in signal transduction pathways for a number of cytokines and growth factors, including GH and PRL. Although these lactogenic hormones have the potential to enhance gonadotropin-induced steroidogenesis, the role of GH and PRL in the testis has long been and remains the subject of controversy. In this report we provide, to our knowledge, the first evidence of Stat5b protein expression in the testis and characterize the activation of Stat5b by these lactogenic hormones in primary rat progenitor, immature and adult Leydig cells, and mouse MA-10 Leydig tumor cells. In MA-10 cells, both GH and PRL mediate tyrosine phosphorylation of Janus kinase (JAK) 2 and Stat5b and induce DNA-binding activity of Stat5b. GH enhances both PIE (PRL-inducible element) and Fc gammaRI gamma-activated sites (GAS), but PRL modulates only PIE GAS. In primary Leydig cells isolated from 18-day-old rats, GH, but not PRL, activates cytoplasmic Stat5b and induces the binding of translocated nuclear Stat5b to GAS elements. Although Stat5b protein is expressed in both Percoll- and elutriator-purified adult rat Leydig cells, neither GH nor PRL treatment results in Stat5b-DNA binding. Our studies indicate that the MA-10 cell has the capacity to bind both GH and PRL and provides a useful model system with which to study the distinct testicular roles of these hormones. Moreover, our findings suggest that progenitor and immature Leydig cells are functional targets for GH in the immature rat, suggestive of a role for GH-Stat5b in testicular development. Our data indicate that lactogenic hormone-inducible transcriptional activation may target distinct gene expression in a signaling cascade(s) involving Stat5b but also imply coordinate control by multiple Leydig cell factors.

Animals↗
PubMed1981

A correlative study of the restorative effects of endogenous and exogenous hormones on the leydig cells, the testis and the epididymis of the regressed hedgehog. Effects of hormones on hedgehog Leydig cells.

The study of the effects of morphogenesis at puberty on the Leydig cells in the testis of the young hedgehog and of the subsequent changes due to the seasonal varisations, has been done. Furthermore, the restorative changes induced by the exogenous hormones in the Leydig cells and the related sex organs of the regressed hedgehogs have also been studied. It was observed that the Leydig cells from the undifferentiated mesenchyme cell-like nature in the young hedgehog, develop into an adult form possessing large number of lipids, a well-developed Golgi apparatus, complex mitochondria and extensive smooth endoplasmic reticulum. The depletion of the lipids and other regression associated changes are found in the interstitial Leydig cells but not in those situated under tunica albuginea and the latter probably function as lipid storing cells during regression. Pituitary extract, either alone or in combination, but not testosterone, could restore completely the structure of the regressed Leydig cells. Similarly, the restoration of the complete process of spermatogenesis and the structure and function of the epididymis in the regressed hedgehog was found to be dependent upon the synergistic action of both testosterone and the gonadotrophic hormones.

Animals↗
PubMed2004

DD-RT-PCR identifies 7-dehydrocholesterol reductase as a key marker of early Leydig cell steroidogenesis.

Postnatal Leydig cell development in rat involves an initial phase of proliferation of progenitor Leydig cells (PLCs) and subsequent differentiation of these cells into immature Leydig cells (ILCs) and adult Leydig cells (ALCs). With an objective to identify the molecular changes associated with Leydig cell differentiation, the mRNA population in PLCs and ILCs were analyzed by the technique of differential display reverse transcription polymerase chain reaction (DD-RT-PCR). Results revealed differential expression of several transcripts in PLCs and ILCs. Of the several differentially expressed transcripts, the expression of transcripts corresponding to collagen IV alpha6 (Col IV alpha6) and ribosomal protein L 41 (RpL41) decreased during the differentiation of PLC to ILC. Also there was an increase in the expression of transcripts encoding enzymes such as microsomal glutathione-S-transferase (mGST 1) and 7-dehydrocholesterol reductase (7-DHCR) during this process. While Col IV alpha6 and RpL41 are known to be involved in cellular proliferation, mGST 1 and 7-DHCR are essential for normal Leydig cell steroidogenesis. A detailed study on 7-DHCR expression in Leydig cells revealed that this enzyme plays a crucial role in steroidogenesis. Interestingly expression of this enzyme is not under acute regulation by Luteinizing hormone (LH).

Animals↗
PubMed1984

Metabolism of androstenedione by Sertoli cell enriched preparations and purified Leydig cells from boar testes in relation to estrogen formation.

The metabolism of [3H]androstenedione in relation to estrogen formation was studied in incubations of Sertoli cell-enriched preparations (30-40% Sertoli cells) and purified Leydig cells (greater than 98%) from testes of mature male pigs. Radioactive metabolites were partitioned by countercurrent distribution (CCD) into unconjugated and 'conjugated' (water-soluble) fractions. Both unconjugated and solvolysed metabolites were separated into neutral and phenolic fractions by CCD with toluene and NaOH. The distribution of radioactivity was examined subsequently for each fraction by partition chromatography on celite columns. Major differences were noted in the products of metabolism from the two cell types. More than half of the radioactivity appeared in the conjugate fraction for Leydig cell incubations, but little or no conjugation occurred in Sertoli cell preparations. Metabolism of androstenedione to other neutral substances was extensive only for Leydig cells, with approx 2% remaining unchanged. No clear evidence of estrogen formation was observed with Sertoli cells; however, both unconjugated and conjugated phenolic for Leydig cell products showed radioactivity corresponding to estrone and estradiol-17 beta on chromatography. About 2-5% of androstenedione was converted to these two estrogens, whereas most of the phenolic material was present as compounds more polar than estradiol.

Androstenedione↗
PubMed1989

[The role of gonadotropins, cyclic AMP, 22-R-OH-cholesterol and cofactors in regulating endocrine functions of the Leydig cells in rats. III. Mechanisms responsible for "desensitization" of the Leydig cells of rats caused by high doses of hCG].

Two groups of rats (a control group and the group examined) were administered intraperitoneally supraphysiological doses of hCG in order to induce a "down regulation" effect on the level of receptors LH and to achieve the desensibilization of Leydig cells. The authors tried to find out at which stage of sequence of changes from receptor stimulation to hormone production there appears a state of cellular resistance to further stimulation. Sections of the nucleus were incubated with various substances influencing steridogenesis (LH, hCG, dbcAMP, 22-R-OH-cholesterol, NAD + NADP + G-6-P + G-6-PDH). An index of the influence of the above substances on the synthesis of androgens were amounts of pregnenolon as the first and testosterone as the final stage of hormonal changes marked radioimmunologically in nucleus homogenates and incubating media. It was shown that the resistance of Leydig cells to further stimulation in the group of animals that were given high doses of hCG is the result of enzymatic blocks in testosterone synthesis. The first block is "late" block of 17 alpha-hydroxylase and 17-20 desmolase, disturbing transforming of 21-carbon steriods into 19-carbon androgens. When the dose of hCG increases, there appears the second block, the so called "early" block, disturbing mitochondrial synthesis of pregnenolon. It was found that exogenic cofactors are in a position, at least partially, to restore the activity of blocked enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehyde-Lyases↗
PubMed1984

Serological and biochemical identification of a plasma membrane antigen specific to Leydig cells.

Purified mouse Leydig cells have been prepared from interstitial cell suspensions using a Percoll gradient procedure. The isolated cells are 88-95% pure as determined by light microscopy. Staining for 3-beta-hydroxysteroid dehydrogenase indicates that over 85% of the Leydig cells recognized by differential interference microscopy are also positive for this enzyme. After separation, the Leydig cells are viable by dye exclusion assays and exhibit normal in situ morphology when examined at the ultrastructural level. Leydig cell suspensions have been used to raise a polyclonal antiserum in rabbits. This antiserum, prior to absorption, reacts in indirect immunofluorescent studies with the surfaces of isolated Leydig cells, with testicular germ cells, with spermatozoa and with somatic cells such as splenocytes. Following absorption with lymphocytes and spermatogenic cells, the antiserum binds only to Leydig cell plasma membranes. Quantitative measurements with 125I-protein A confirm the specific labeling of Leydig cells by the absorbed antiserum. Biochemical identification of the Leydig cell plasma membrane antigen has been accomplished by immunoblotting polyacrylamide gel nitrocellulose transfers. A single major band of Mr approximately 40,000 is detected on one-dimensional transfers; two weakly reactive spots of Mr 43,000 and 45,000 are detected using two-dimensional immunoblots. Blotting experiments conducted using concanavalin A have identified the major Leydig cell constituents reactive with this lectin. The Leydig cell plasma membrane antigen(s) does not bind concanavalin A.

3-Hydroxysteroid Dehydrogenases↗
PubMed1996

[Alteration of mRNA transcripts of rat Sertoli cell secreted proteins and Leydig cell LH/CG-R protein following glycosides of Tripterigium Wilfordii Hook administration].

Our studies were undertaken to assess the male antifertility mechanism of the total glycosides extracted from Tripterigium Wilfordii Hook. f. (GTW). In experimental group I, GTW was given by gastric gavage at a dose of 30 mg/kg per day for 35 days. In experimental group I, GTW was given in the same way at a dose of 10 mg/kg per day for 49 days. The transcripts level analysis indicated that in all the experimental groups ABP, SGP-2 and LH/CG-R mRNA were increased. Two ABP and two LH/CG-R mRNA transcripts with respective molecular sizes of 1.7 kb, 2.3 kb and 1.2 kb, 4.4 kb were identified. ABP and LH/ CG-R mRNA with 1.7 kb and 1.2 kb increased, while those with 2.3 and 4.4 kb remained unchanged. In addition, the changes of different proteins at the mRNA level were shown to be GTW dose-dependent. The morphological features of germ cell degeneration and appearance of germ cells in tubular lumen suggest that the increases in transcripts level of three proteins in testis may not be directly associated with the effect of GTW. The question whether GTW interfere with the function of sertoli cells and leydig cells would be study.

Androgen-Binding Protein↗
PubMed2004

Nestin, a neuroectodermal stem cell marker molecule, is expressed in Leydig cells of the human testis and in some specific cell types from human testicular tumours.

The intermediate filament protein nestin is predominantly expressed in some stem/progenitor cells and appears to be a useful molecular tool to characterise tumours originating from precursor cells of neuroectodermal and mesenchymal lineages. Leydig cells originate in the adult testis by differentiation from stem cells and express a variety of neural and neuroendocrine markers. The possible expression of the neural stem cell marker nestin in Leydig cells and testicular tumour cells was determined by analysing the patterns of nestin expression in normal and pathological human testes by Western blot and immunohistochemical methods. In normal testis, nestin was found in some vascular endothelial cells, a subset of peritubular spindle-shaped cells and some Leydig cells; spermatogenic and Sertoli cells were unstained. In normal Leydig cells, nestin was distributed in the perinuclear cytoplasm and accumulated in the crystalloids of Reinke with ageing. In non-tumour pathologies (cryptorchidism, impaired spermatogenesis), the seminiferous tubules were immunonegative, whereas hyperplastic Leydig cells showed cytoplasmic immunolabelling. In testicular malignancies, nestin was localised in the Sertoli cells of the seminiferous tubules affected with intratubular germ cell neoplasia, in the hyperplastic Leydig cells associated with these tumours and in some components (mesenchymal and neuroepithelial cells) of teratomas; spermatocytic and non-spermatocytic seminomas were unstained. Some vascular endothelial cells were immunolabelled in all tumour samples. Thus, nestin is expressed in a population of normal and hyperplastic Leydig cells and in Sertoli cells in the presence of intratubular germ-cell neoplasia. Nestin may be a good marker for identifying components of testicular teratomas.

Adolescent↗
PubMed2006

Ultrastructure of cell contacts of fetal and adult Leydig cells in the rat: a systematic study from birth to senium.

Differentiation, development, and function of Leydig cells in the testis are regulated also by macrophages, vascular endothelial cells, and peritubular cells in the testis. The aim of the present study was to investigate the possible morphological substrates for communication between these cells. The cell contacts between adjacent Leydig cells, and between Leydig cells and other interstitial cells were studied electron microscopically in the rat testis of various age groups from birth to senium. Intercellular bridges with continuous cytoplasm were observed between fetal Leydig cells (FLCs) in the early postnatal period. Gap junctions were present in nearly every age group. A structural diversity as well as an increased occurrence of gap junctions with the maturity of the Leydig cells was noted. Coated pits were observed initially on pnd 30. From pnd 50 onwards, macrophages and Leydig cells were attached very closely to each other, when the cell processes of Leydig cells protruded either into the coated pits or into the deep invaginations of macrophages. To conclude, this is the first report on the presence of intercellular bridges between FLCs suggesting a possible functional synchronization of interconnected Leydig cells. The cell contacts observed here are possibly required for a precise communication between the Leydig cells and other interstitial cells.

Animals↗