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PubMed1999

Hepatocytic differentiation in retiform Sertoli-Leydig cell tumors: distinguishing a heterologous element from Leydig cells.

Sertoli-Leydig cell tumors (SLCT) of the ovary are rare sex cord-stromal neoplasms. A minority of SLCT are characterized by a pattern resembling that of the rete ovarii and frequently have a range of homologous and heterologous tissues. Approximately 20 cases of SLCT have been reported to have elevation of serum alpha-fetoprotein (AFP) levels, or tissue immunoreactivity for AFP, a protein usually associated with germ cell neoplasms, especially yolk sac tumor. We identified hepatocytic differentiation in five cases of retiform SLCT (RSLCT), and confirmed immunohistochemically that these cells are hepatocytes rather than Leydig cells. Hepatocytes are positive for keratins (AE1/3 and Cam 5.2), AFP, and ferritin, negative for vimentin, and show weak to moderate staining for inhibin. Leydig cells are negative for keratins, positive for vimentin, and intensely positive for inhibin. Immunohistochemistry is needed to distinguish hepatocytic differentiation from Leydig cells with certainty. Including the cases in this report, hepatocytic differentiation has been associated with a retiform pattern in SLCT in 14 of 25 cases (56%). The association of these two patterns appears to be characteristic of a relatively primitive sex cord-stromal neoplasm.

Adolescent↗
PubMed1999

Transforming growth factor beta signal transducer Smad2 is expressed in mouse meiotic germ cells, Sertoli cells, and Leydig cells during spermatogenesis.

Although previous studies have shown that members of the transforming growth factor beta (TGFbeta) family are expressed in the seminiferous tubules, the functions of these growth factors in spermatogenesis remain elusive. In order to shed light on the mechanisms of TGFbeta action in spermatogenesis, it is crucial to determine whether and where their downstream signaling molecules are expressed in the testis. We examined the expression of Smad2, an intracellular signal transducer of the TGFbetas, in mouse testes by in situ hybridization and immunohistochemistry. Both Smad2 mRNA and protein were detected in meiotic germ cells, from preleptotene to pachytene spermatocytes, but not in postmeiotic germ cells. Smad2 expression was also observed in interstitial cells and Sertoli cells. Therefore, our data provide molecular evidence for TGFbeta signal transduction during spermatogenesis.

Animals↗
PubMed1985

Morphological and functional characteristics of rat Leydig cells isolated on Percoll gradients: is Leydig cell heterogeneity in vitro an artifact?

Rat testicular intertubular cells have been isolated on Percoll density gradients. Detailed light and electron microscopic studies have determined the sedimentation positions for Leydig cells, macrophages, fibroblasts, endothelial cells, germ cells and residual bodies. Stereological techniques have been utilized to determine the number of cells in the region of the gradient where Leydig cells sediment. Morphologically intact Leydig cells were present in the more dense region of the gradient (1.0590-1.0900 g/ml), and they responded to hCG stimulation with an 11-fold increase in testosterone production and contained LH/hCG receptors. Leydig cells in the less dense region of the gradient (1.0440-1.0589 g/ml) secreted less testosterone and contained less hCG receptors than those obtained from denser regions. However, the morphological studies described herein provide evidence for the first time that the majority of these less functional 'Leydig cells' from the lighter region of the gradients do not contain a nucleus and represent pieces of Leydig cell cytoplasm with variable size, shape and complement of organelles.

Animals↗
PubMed1994

Identification of a cyclic adenosine 3',5'-monophosphate-response element in the rat aromatase promoter that is required for transcriptional activation in rat granulosa cells and R2C leydig cells.

Cytochrome P450 aromatase, which converts testosterone to estradiol, is transcriptionally induced by FSH and cAMP during ovarian follicular development. At least one promoter element [-82/-31 base pairs (bp)] required for stimulation of the rat gene in granulosa cells binds steroidogenic factor-1, an orphan steroid receptor. In this paper, we demonstrate that an additional region, -161/-138 bp is required for cAMP regulation. This region shares homology with promoter sequences in the bovine 21-hydroxylase and mouse 11 beta-hydroxylase genes that are also induced by cAMP, yet each binds different proteins in granulosa cell nuclear extracts. The aromatase -161/-138 bp region contains a cAMP-response element (CRE)-like sequence, TGCACGTCA. Deletion or mutation of this sequence reduces promoter activity of chimeric chloramphenicol acetyl transferase (CAT) reporter constructs that are transiently transfected into granulosa cells and R2C Leydig cells. Granulosa cell nuclear proteins and R2C cell nuclear proteins specifically bind the -161/-138 bp region and form three protein/DNA complexes. Recombinant CRE-binding protein (CREB) binds the CRE-like sequence and forms a single band, and a CREB antibody retards the migration of CREB and one granulosa cell protein-aromatase DNA binding complex. Using Western blot analysis, CREB was demonstrated in granulosa cell nuclear extracts from all stages of follicular development. Thus, aromatase is transcriptionally regulated by a hexameric sequence binding SF-1 and a CRE sequence binding CREB and other factors present in granulosa cells and in R2C Leydig cells. The presence of identical SF-1 and CRE-like sequences in the human ovarian aromatase promoter II suggests that the human promoter may also be regulated in a similar manner.

Animals↗
PubMed1984

Leydig cell hyperplasia in cryptorchid patients: quantitative evaluation of Leydig cells in undescended and contralateral scrotal testes.

Leydig cell number was evaluated quantitatively in testicular biopsies from post-pubertal cryptorchid patients and normal controls. For this quantitative evaluation we used the following method. This is based on the determination of the total number of Leydig cells, Leydig cell clusters and seminiferous tubules in the entire histologic sections of each biopsy and the determination of the following indices; mean Leydig cells per tubule, mean Leydig cell clusters per tubule and mean Leydig cells per cluster. In addition, the numbers of Sertoli cells were counted, and Leydig-Sertoli cell ratio was also determined. These indices were correlated with each other. All indices were significantly elevated not only in undescended but in contralateral scrotal testes of the cryptorchid patients in comparison to those in normal controls. Between undescended and descended scrotal testes of the same individual patients, those indices were significantly higher in the descended scrotal testes than in the undescended ones. Thus, Leydig cell hyperplasia was noted in the testes of post-pubertal cryptorchid patients, and was more prominent in the contralateral scrotal testes than in the undescended ones.

Adolescent↗
PubMed1981

The aging Leydig cell: 2. Two distinct populations of Leydig cells and the possible site of defective steroidogenesis.

Using metrizamide gradient centrifugation two populations of Leydig cells were found in both 60-90 day-old and 24 month-old rats. Cells from both Band 2 (B2) and Band 3 (B3) responded to LH stimulation with increased cyclic AMP formation; however, only B3 cells produced significant amounts of testosterone. Cells from both B2 and B3 of the old rats synthesized less cyclic AMP and testosterone than cells from their younger counterparts. In response to LH stimulation, 0.01 - 1.0 mIU/ml, no appreciable difference of cyclic AMP formation could be detected between young and old Leydig cells. Maximal testosterone production occurred when 1 mIU/ml LH was used. Only when LH concentration was increased to 10 and 100 mIU/ml, did young Leydig cells produce significantly more cyclic AMP than old Leydig cells. After addition of 5X10(-7)M of pregnenolone or progesterone to the incubation medium, both young and old Leydig cells produced comparable amounts of testosterone. These results demonstrate no impairment of old rat Leydig cells to synthesize testosterone from pregnenolone and progesterone.

Aging↗
PubMedDate not supplied

Regulatory cytokine expression and interstitial fluid formation in the normal and inflamed rat testis are under leydig cell control.

Leydig cells have been implicated in several inflammation-related responses of the testis. Specifically, these cells produce the proinflammatory cytokines interleukin-1 (IL-1) and IL-6, stimulate macrophage recruitment, and promote interstitial fluid formation. In addition, the immunoregulatory cytokines macrophage migration inhibitory factor (MIF), transforming growth factor-beta1 (TGFbeta1), and interferon-gamma (IFNgamma) are constitutively expressed by testicular cells, including the Leydig cells. In the present study, the contribution of the Leydig cell to testicular inflammatory responses was examined in adult male rats treated with the Leydig cell-specific toxin, ethane dimethane sulfonate (EDS). Intratesticular testosterone levels were modulated by subcutaneous testosterone implants. After 10 days, animals received an injection of lipopolysaccharide (LPS) to induce an inflammatory response, or saline alone, and were killed 3 hours later. Both depletion of Leydig cells by EDS and LPS treatment caused a decrease in collected testicular interstitial fluid to about 35% of control levels, but the effects were not additive. Maintenance of intratesticular testosterone reversed the interstitial fluid decline following EDS treatment and partially prevented the LPS-induced effect. MIF, TGFbeta1, and IFNgamma were expressed in both the normal and inflamed testis at similar levels. In contrast, EDS treatment caused a significant decline in expression of all 3 cytokines, which was prevented by the testosterone implants. These data indicate that 1) expression of TGFbeta1, MIF, and IFNgamma in the testis is not dependent on the presence of intact Leydig cells but is under direct testosterone control and 2) the decline in testicular interstitial fluid during inflammation involves the Leydig cells, acting via both androgens and nonandrogenic secretions. These data provide further support for a significant role for the Leydig cell in modulating the testicular response to inflammation.

Animals↗
PubMed1998

Mesonephric stromal cells differentiate into Leydig cells in the mouse fetal testis.

Circumstantial evidence has suggested that Sry expression probably occurs in pre-Sertoli cells, implying that they produce signals required for testis differentiation. From experiments involving gonad/mesonephros grafts it has been shown that, at 11.5 days postcoitum stromal cells from the mesonephros invade the male gonad. Although in the grafted testes, Leydig cells appeared among the stromal cells, in these studies their origin remained elusive. In the current study, we reconstructed urogenital ridges in organ culture by grafting morphologically undifferentiated male genital ridges from CD-1 embryos, to mesonephroi from ROSA26 transgenic embryos whose cells express the bacterial beta-galactosidase. With an improved technique for the detection of beta-gal enzyme activity in electronmicrographs, we studied cell migration and differentiation of mesonephric cells into the testis in reconstructed urogenital ridges with XY or XX mesonephroi. It was found that, in addition to differentiation of myoid and connective cells, some migratory mesonephric cells acquired ultrastructural features of steroidogenic Leydig cells. Several beta-gal positive cells differentiated as Leydig cells in gonads grafted with either male or female mesonephros. The results suggest that mesonephric cells responded to putative signal(s) produced in the male gonad and participate in morphogenesis and cell differentiation of the fetal testis.

Animals↗
PubMed1986

Cross-reactivity of a monoclonal antibody directed against an estrogen-induced protein in MCF-7 human breast cancer cells with murine Leydig cell tumor proteins.

An estrogen-responsive murine Leydig cell tumor (M5480A) was examined for the presence of cross-reactive proteins to a monoclonal antibody directed against a Mr 24,000 estrogen-regulated protein in human breast cancer cells. Human breast tumor biopsies were used as controls for the cytosol preparations, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and Western blot conditions used in these experiments. The estrogen-regulated Mr 24,000 protein was detected in sodium dodecyl sulfate-polyacrylamide gels of cytosols from four human breast tumor biopsies examined. Larger amounts of the Mr 24,000 protein were present in the two estrogen-progesterone receptor-positive tumor biopsies in comparison to the two estrogen-progesterone receptor-negative samples. In addition, the two receptor-positive samples demonstrated an additional, less intense immunoreactive band at Mr 21,000. Under identical conditions, the same monoclonal antibody bound to two major protein bands from sodium dodecyl sulfate-polyacrylamide gels of Leydig cell tumor cytosols at Mr 56,000 and Mr 86,000. Antibodies prepared from BALB/c mouse ascites fluid of animals bearing the parent myeloma cell line (P3X63NS1) exhibited no immunoreactivity against the human breast or Leydig cell tumor proteins. In light of the high degree of specificity which this monoclonal antibody exhibits, our results suggest that similar antigenic determinants may exist in these proteins from two distinct tumors.

Animals↗
PubMed1989

Proliferation and differentiation of possible Leydig cell precursors after destruction of the existing Leydig cells with ethane dimethyl sulphonate: the role of LH/human chorionic gonadotrophin.

The influence of LH levels on the proliferation and differentiation of possible Leydig cell precursors was investigated in adult rats, after the destruction of the existing Leydig cells with the cytotoxic drug ethane dimethyl sulphonate (EDS). In rats bearing a testosterone implant which prevented the rise in plasma LH levels and kept them within the normal range after the destruction of the Leydig cells, the proliferative activity of possible Leydig cell precursors still increased seven- to eightfold 2 days after EDS administration. Apparently, in this situation, locally produced factors, and not LH, may play a role in the stimulation of proliferation. The proliferative activity of the possible precursor cells could be further stimulated by treating rats with daily injections of human chorionic gonadotrophin (hCG) following EDS administration. It was concluded that the proliferative activity of possible Leydig cell precursors is probably regulated by both paracrine and endocrine factors. Almost no Leydig cells were formed in the rats bearing a testosterone implant during the first 4 weeks after EDS administration. When these rats were treated with hCG, starting 28 days after administration of EDS, a substantial number of Leydig cells was found after 2 days, and these cells also showed 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and alpha-naphtyl esterase (alpha-NE) activity. When hCG treatment was started at 14 or 21 days after EDS administration, some cells with the nuclear characteristics of Leydig cells were present after 2 days, but no 3 beta-HSD or alpha-NE activity could be detected.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxysteroid Dehydrogenases↗