Endothelin Stimulates Testosterone Secretion by Rat Leydig Cells

Conte, D.; Questino, P.; Fillo, Silvia; Nordio, Maurizio; Isidori, Aldo; Romanelli, Francesco

doi:10.1677/joe.0.136r001

Cited by 35 publications

(23 citation statements)

References 14 publications

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“…Our results are partially at variance with those of Filippini et al [15], who did not observe the presence of Ca 2+ influx in cultured TPMC. The underlying reasons in that study for a Ca 2+ response in TPMC to ET-1 so different from that of other vascular smooth muscle cells (VSMC), and from what we observed in TPMC, are difficult to assess; but one important factor might be that that study was performed on single attached cells, an experimental model characterized by a great degree of variability in cellular Ca 2 + response [32].…”

supporting

confidence: 53%

“…High-affinity receptors with the binding characteristics of ETA receptors are present in Leydig cells [12] and in the MA-10 murine Leydig tumor cell line [14]. In both cell types, ET-1 stimulates steroidogenesis, increasing basal and hCG-stimulated testosterone production in the former [15] and progesterone release in the latter [141. Autoradiographic studies have localized ET receptors in the testis also at the level of peritubular myoid cells [9,11], and it has recently been shown that these cells bind ET-1 with subsequent rapid intracellular Ca 2+ increase and production of inositol triphosphate [16].…”

Section: Introductionmentioning

confidence: 99%

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Endothelin-1 Stimulates Deoxyribonucleic Acid Synthesis and Contraction in Testicular Peritubular Myoid Cells1

Santiemma¹,

Beligotti²,

Magnanti³

et al. 1996

Biology of Reproduction

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In the testis, endothelin-1 (ET-1) is produced by Sertoli cells, and it has been proposed to be a paracrine factor participating in the regulation of tubular and interstitial function. The response of purified testicular peritubular myoid cells (TPMC) to ET-1 was investigated in the present study. TPMC expressed a single class of high-affinity receptors that were shown by competitive binding experiments with sarafotoxin-6c to belong to the ETA subtype. The binding of ET-1 to TPMC was followed by rapid internalization of the receptor-ligand complex. ET-1 induced a prompt rise in intracellular Ca2+ concentration that was blunted in Ca(2+)-free medium and in the presence of Mn2+ or of voltage-operated-calcium-channel (VOC) blockers, indicating that both Ca2+ mobilization from intracellular stores and extracellular Ca2+ influx were involved. Thymidine uptake was promoted by ET-1 in a time-dependent manner, and the use of cyclo[D-Asp-L-Pro-D-Val-L-Leu-D-Trp] (BQ123) reduced the incorporation of thymidine. Protein kinase C (PKC) inhibition (100 nM calphostin C) abolished the ET-1 mitogenic effect. ET-1 also promoted TPMC contraction, as evaluated in collagen lattices, in a dose-related manner, with the half-maximal response observed at 1 nM. As in the case of mitogenesis, BQ123 blunted ET-1-induced contraction. PKC inhibition abolished ET-1-induced contraction. These findings indicate that ET-1 promotes DNA synthesis and contraction of TPMC and that both effects are mediated by PKC; they suggest as well that ET-1 may have a physiological role in the interaction between Sertoli cells and TPMC.

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supporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Endothelin-1 Stimulates Deoxyribonucleic Acid Synthesis and Contraction in Testicular Peritubular Myoid Cells1

Santiemma¹,

Beligotti²,

Magnanti³

et al. 1996

Biology of Reproduction

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“…Moreover, germ cell opioids [49] may be involved in the local control of Sertoli cell secretion of an argininevasopressin-like peptide that in turn regulates Leydig cell production of testosterone [50]. The demonstration that the germ cell 03-fibroblast growth factor is implicated in the regulation of rat Sertoli cell transferrin output [51] and the recent report of Onoda and Djakiew [43] showing that a 29-kDa protein isolated from round spermatids stimulates rat Sertoli cell transferrin synthesis raise questions about the exact nature of the germ cell paracrine factor(s) involved in the regulation of the synthesis of Sertoli cell transferrin as well as the paracrine factor involved in the control of Leydig cell testosterone synthesis [48,52,53].…”

Section: Discussionmentioning

confidence: 99%

Evidence for Germ Cell Control of Sertoli Cell Function in Three Models of Germ Cell Depletion in Adult Rat

Boujrad

Reviers

Carreau

1995

Biology of Reproduction

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In order to clarify the role of germ cells in the regulation of Sertoli cell secretions, three experimental models of germ cell depletion were used: hypodactyl rat mutation (testis weight [TW]: 55% less than controls), in utero busulfan treatment (TW: 88% less than controls), and neonatal experimental cryptorchidism (TW: 72% less than controls). The aim of this work was to compare the numbers of Leydig and Sertoli cells and the production of germ cells in each experimental model to the in vitro secretions of Leydig and Sertoli cells in conditioned media and to the hormonal serum profiles of the same animal in vivo. In the three models, serum levels of hypophyseal and testosterone hormones were significantly increased and decreased, respectively. In the absence of germ cells, the total length of seminiferous tubules, the total numbers of Sertoli and Leydig cells, and the daily production of germ cells were significantly diminished. The addition of both control and damaged seminiferous tubule culture media (STM: media conditioned by 10 cm of seminiferous tubules) to 10(6) control or damaged Leydig cells led to a further increase of testosterone production after ovine LH stimulation. However, expressed per Sertoli cell, testosterone production by control Leydig cells was reduced by addition of damaged STM as compared to addition of control STM, and similarly, the addition of control STM to damaged Leydig cells enhanced testosterone production more than did the addition of damaged STM. Secretions of transferrin per Sertoli cell in STM were reduced as compared to controls by the absence of germ cells but to a lesser extent than was production of spermatocytes and of spermatids. In conclusion, secretions by Sertoli cells of the paracrine factor involved in the control of testosterone production by Leydig cells and of transferrin are modified by germ cells.

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“…All experiments were performed soon after the death of the rat, which took place at 0900 h. Leydig cell purification was performed as previously described (Conte et al 1993). Immediately after death, the testes were removed and infused, via the testicular artery, with an enzyme solution (collagenase 0·5 mg/ml, soybean trypsin inhibitor 0·2 mg/ml, and leupeptin 5 µg/ml in HBSS containing 0·1% (wt/vol) BSA, pH 7·4) and then dispersed in enzyme solution in a shaking waterbath (20 min; 90 cycles/min; 34 C).…”

Section: Leydig Cell Purificationmentioning

confidence: 99%

A novel mechanism for the melatonin inhibition of testosterone secretion by rat Leydig cells: reduction of GnRH-induced increase in cytosolic Ca2+

Valenti¹,

Thellung²,

Florio³

et al. 1999

Journal of Molecular Endocrinology

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The site of inhibition, by melatonin, of GnRHdependent testosterone secretion was investigated in adult rat Leydig cells cultured in vitro. The various effects downstream of the binding of GnRH to its own receptor were isolated and mimicked by specific drugs. Testosterone secretion was then evaluated after 3 h stimulation with GnRH, thapsigargin (1 µM), phorbol-12-myristate-13-acetate (100 nM), arachidonic acid (20 µM), and ionomycin (1 µM) in the presence or absence of melatonin (215 nM). The effect of melatonin on the GnRH-induced changes in cytoplasmic calcium concentration ([Ca 2+ ] i ) was also studied, using Fura-2 as fluorescent Ca 2+ indicator. Melatonin attenuated the increase in [Ca 2+ ] i and inhibited the testosterone secretion induced by GnRH, but not that induced by ionomycin. Both ionomycin and thapsigargin potentiated GnRH-induced testosterone secretion; however, ionomycin, but not thapsigargin, partially prevented the inhibitory effect of melatonin on cells stimulated with GnRH. The effect of melatonin was probably dependent on the binding of melatonin to its Gi-protein-coupled receptor, as the inhibitory effect on GnRH-induced secretion was supressed in cells pretreated with pertussis toxin in a concentration of 180 ng/ml for 20 h. Assay of 17-hydroxy-progesterone showed that, irrespective of the treatment, cells cultured with melatonin secreted greater amounts than controls. We conclude that melatonin reduces GnRH-induced testosterone secretion by 1) decreasing [Ca 2+ ] i , through impairment of the GnRH-dependent release of Ca 2+ from intracellular stores and 2) blocking 17-20 desmolase enzymatic activity, an effect that occurs irrespective of changes in [Ca 2+ ] i .

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Endothelin Stimulates Testosterone Secretion by Rat Leydig Cells

Cited by 35 publications

References 14 publications

Endothelin-1 Stimulates Deoxyribonucleic Acid Synthesis and Contraction in Testicular Peritubular Myoid Cells1

Endothelin-1 Stimulates Deoxyribonucleic Acid Synthesis and Contraction in Testicular Peritubular Myoid Cells1

Evidence for Germ Cell Control of Sertoli Cell Function in Three Models of Germ Cell Depletion in Adult Rat

A novel mechanism for the melatonin inhibition of testosterone secretion by rat Leydig cells: reduction of GnRH-induced increase in cytosolic Ca2+

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