Regulation of inhibin secretion by Sertoli cell-enriched cultures

1983 ◽  
Vol 102 (1) ◽  
pp. 136-143 ◽  
Author(s):  
G. Verhoeven ◽  
P. Franchimont

Abstract. Sertoli cells secrete a factor which has the same bioactivity as ovine testicular lymph inhibin: it selectively suppresses the secretion of FSH by cultured pituitary cells. We investigated the factors that acutely modulate the secretion of this inhibin by cultured Sertoli cells derived from immature rats. The secretion of inhibin was studied on day 7 of culture after a 24 h period of incubation in the presence or absence of steroids, gonadotrophins and foetal bovine serum, added alone or in various combinations. It could be demonstrated that aromatisable as well as non-aromatisable natural and synthetic androgens promote the secretion of inhibin in a dose-dependent way. FSH and pregnant mare serum gonadotrophin — at concentrations that clearly stimulate Sertoli cell aromatase activity — did not affect basal or androgen-stimulated production of inhibin. hCG was equally uneffective. The effect of androgens was not modified by the addition of an aromatase inhibitor but it was neutralized by the antiandrogen cyproterone acetate. Oestradiol-17β did not influence the secretion of inhibin whereas progesterone decreased it. Serum enhanced basal as well as androgen stimulated secretion of inhibin. It is concluded that androgens are the major factor which acutely stimulates the production of Sertoli cell inhibin.

1986 ◽  
Vol 108 (1) ◽  
pp. R1-R3 ◽  
Author(s):  
N. Jenkins ◽  
J.D. Ellison

ABSTRACT Bovine FSH stimulated a six fold increase in secretion of plasminogen activator by immature bovine Sertoli cells with half-maximum response (ED50) at 145ng/ml. Treatment with FSH and either dexamethasone, cortisol or corticosterone produced a dose-dependent suppression of PA activity, with ED50 values of 35, 320 and >650nmol/l respectively. Effects of dexamethasone required over 6 h incubation to become significant (P < 0.001), and were blocked by inhibitors of RNA synthesis and translation. These data demonstrate direct effects of corticosteroids on Sertoli cells, resulting in the synthesis of antiprotease factors which antagonize the actions of FSH.


1994 ◽  
Vol 140 (3) ◽  
pp. 431-436 ◽  
Author(s):  
S Ulisse ◽  
E A Jannini ◽  
E Carosa ◽  
D Piersanti ◽  
F M Graziano ◽  
...  

Abstract Basal and FSH-induced aromatase activity in prepubertal rat Sertoli cells was inhibited by l-tri-iodothyronine (T3) in a time- and dose-dependent manner. The effect was evident only after 6 h of preincubation with T3 (10−7 m) and the half-maximal dose was 0·5 ±0·2 nm, which correlated with the Kd of the nuclear T3 receptor of rat Sertoli cells (Kd=1–2 nm). The effect was specific as judged by the lack of effect of the T3 analogue 3-iodo-l-thyrosine. The inhibitory effect of T3 was present over the entire range of FSH concentrations used (0·001–100 ng/ml). In T3-treated Sertoli cells, aromatase activity induced by 8-bromo-cyclic AMP was inhibited by the same order of magnitude as that of FSH, thus suggesting that the inhibitory effect of T3 was downstream from cyclic AMP formation. Furthermore, pretreatment of Sertoli cells cultures with T3 (24 h, 10−7 m) did not affect basal or FSH-induced extracellular cyclic AMP accumulation. This effect of T3 on rat Sertoli cell aromatase activity may be regarded as a part of the integrated mechanism by which thyroid hormone modulates the functions of the seminiferous epithelium. Journal of Endocrinology (1994) 140, 431–436


1995 ◽  
Vol 145 (2) ◽  
pp. 355-362 ◽  
Author(s):  
S Palmero ◽  
M Prati ◽  
F Bolla ◽  
E Fugassa

Abstract The addition of physiological concentrations (1 nm) of tri-iodothyronine (T3) to the culture medium of Sertoli cells from prepubertal (8-day-old) rats stimulated both protein synthesis (+55%) and lactate (+50%) production, while it inhibited DNA synthesis (−30/35%) and aromatase activity (−45/50%); insignificant T3-dependent effects were observed in cultured Sertoli cells from midpubertal (28-day-old) rats. These data suggest an age-dependent role for thyroid hormone in promoting and maintaining Sertoli cell differentiation at puberty; moreover, the hormone is involved in the regulation of Sertoli cell proliferation. The present study validates the role of Sertoli cells as a specific target for T3 action at the testis level; it also demonstrates the existence of an early and critical direct influence of thyroid hormone on Sertoli cell proliferation and functional maturation. Journal of Endocrinology (1995) 145, 355–362


Endocrinology ◽  
2020 ◽  
Vol 161 (7) ◽  
Author(s):  
Penny A F Whiley ◽  
Liza O’Donnell ◽  
Sarah C Moody ◽  
David J Handelsman ◽  
Julia C Young ◽  
...  

Abstract Activin A promotes fetal mouse testis development, including driving Sertoli cell proliferation and cord morphogenesis, but its mechanisms of action are undefined. We performed ribonucleic acid sequencing (RNA-seq) on testicular somatic cells from fetal activin A-deficient mice (Inhba KO) and wildtype littermates at embryonic day (E) E13.5 and E15.5. Analysis of whole gonads provided validation, and cultures with a pathway inhibitor discerned acute from chronic effects of altered activin A bioactivity. Activin A deficiency predominantly affects the Sertoli cell transcriptome. New candidate targets include Minar1, Sel1l3, Vnn1, Sfrp4, Masp1, Nell1, Tthy1 and Prss12. Importantly, the testosterone (T) biosynthetic enzymes present in fetal Sertoli cells, Hsd17b1 and Hsd17b3, were identified as activin-responsive. Activin-deficient testes contained elevated androstenedione (A4), displayed an Inhba gene dose-dependent A4/T ratio, and contained 11-keto androgens. The remarkable accumulation of lipid droplets in both Sertoli and germ cells at E15.5 indicated impaired lipid metabolism in the absence of activin A. This demonstrated for the first time that activin A acts on Sertoli cells to determine local steroid production during fetal testis development. These outcomes reveal how compounds that perturb fetal steroidogenesis can function through cell-specific mechanisms and can indicate how altered activin levels in utero may impact testis development.


1998 ◽  
Vol 157 (2) ◽  
pp. 275-283 ◽  
Author(s):  
SB Meroni ◽  
DF Canepa ◽  
EH Pellizzari ◽  
HF Schteingart ◽  
SB Cigorraga

To study the role of extracellular nucleosides and nucleotides in the regulation of Sertoli cells, the effects of agonists which occupy A1 and P2 purinergic receptors on aromatase and gamma-glutamyl transpeptidase (gamma-GTP) activities and on transferrin secretion were tested. Sertoli cell treatment with purinergic agonists for a prolonged period of time (72 h) resulted in an increase in aromatase activity under basal conditions. In cultures stimulated with FSH, purinergic agonists counteracted the inhibitory effect on aromatase activity that long-term treatment with FSH promoted. The effects of prolonged treatments with purinergic agonists on the other two parameters of Sertoli cell function were less pronounced. Neither gamma-GTP activity nor transferrin secretion was modified under basal conditions. On the other hand, under conditions where cell differentiation was favored by FSH treatment, reductions in gamma-GTP activity and transferrin secretion were usually observed. The results obtained in dbcAMP-stimulated cultures suggested that A1 agonists exert their regulatory function at the level of cAMP formation while P2 agonists act at a more distal point. The fact that morphological changes induced by FSH were reversed by both types of agonists, while those induced by dbcAMP were only abrogated by P2 agonists, supports this hypothesis. In summary, these results demonstrate that purinergic agonists may be important in the regulation of Sertoli cell function.


1989 ◽  
Vol 121 (2) ◽  
pp. 265-269 ◽  
Author(s):  
M. Simoni ◽  
S. A. Khan ◽  
Ch. De Geyter ◽  
E. Nieschlag

Abstract. Effects of serum from pregnant women on basal and FSH (or cAMP) stimulated aromatase activity of immature rat Sertoli cells in primary culture were studied. Pregnancy serum caused a dose-dependent stimulation of Sertoli cell aromatase activity and the response curves were parallel to those obtained with human FSH. This stimulatory (FSH-like) activity increased progressively during pregnancy, with a sharp drop immediately after delivery. However, the FSH-like bioactivity was not associated with immunoreactive FSH when a specific radioimmunoassay was employed. On the other hand, serum from pregnant women caused a dose-dependent inhibition of FSH and dibutyryl-cAMP-stimulated aromatase activity. These data suggest that human pregnancy serum contains factor(s) which may stimulate basal aromatase activity of Sertoli cells and may inhibit FSH-induced aromatase activity. These factors, most probably of placental origin, may play a role in the regulation of estrogen production during gestation.


1980 ◽  
Vol 84 (3) ◽  
pp. 333-341 ◽  
Author(s):  
TAKAHIDE MORI ◽  
HEIGO KOHDA ◽  
YASUSHI KINOSHITA ◽  
YOJIRO EZAKI ◽  
NORIHIKO MORIMOTO ◽  
...  

Treatment of immature rats with pregnant mare serum gonadotrophin followed by human chorionic gonadotrophin (HCG) caused an acute and temporary increase in concentrations of progesterone, testosterone and oestradiol in plasma with maximum levels 3 h after the administration of HCG. Concurrent injection of indomethacin and HCG reduced, in a dose-dependent manner, the mean number of ova shed and this was accompanied by a dose-dependent decrease in concentrations of plasma progesterone and testosterone but not of oestradiol when they were measured 3 h after the injection of HCG. The minimum effective dose that blocked ovulation completely at 0 h abolished the acute increase of progesterone and testosterone, suggesting that prostaglandins act on ovulation by stimulating steroidogenesis at an early stage in the preovulatory process. The anti-ovulatory action of the minimum effective dose at 0 h became progressively less potent as the time between injection of HCG and administration of indomethacin was increased, although plasma concentrations of progesterone and testosterone measured at autopsy 18 h after treatment with HCG had not changed appreciably. When indomethacin was administered 10 h after HCG, the relationship between the dose of indomethacin and the mean number of ova differed from that observed when simultaneous injections of indomethacin and HCG were given, and the minimum effective dose that prevented ovulation was much higher than that at 0 h, suggesting that prostaglandins act differently on ovulation in the later stage of the preovulatory process. It was concluded that prostaglandins may mediate the action of HCG on ovulation through two mechanisms which operate at different stages of the preovulatory process.


Author(s):  
Rita Meyer ◽  
Zoltan Posalaky ◽  
Dennis Mcginley

The Sertoli cell tight junctional complexes have been shown to be the most important structural counterpart of the physiological blood-testis barrier. In freeze etch replicas they consist of extensive rows of intramembranous particles which are not only oriented parallel to one another, but to the myoid layer as well. Thus the occluding complex has both an internal and an overall orientation. However, this overall orientation to the myoid layer does not seem to be necessary to its barrier function. The 20 day old rat has extensive parallel tight junctions which are not oriented with respect to the myoid layer, and yet they are inpenetrable by lanthanum. The mechanism(s) for the control of Sertoli cell junction development and orientation has not been established, although such factors as the presence or absence of germ cells, and/or hormones, especially FSH have been implicated.


2009 ◽  
Vol 6 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Yang Li ◽  
Wang Xian-zhong ◽  
Yang Meng-bo ◽  
Zhang Jia-hua

AbstractTo illustrate the effect of nitric oxide (NO) on the microtubules of Sertoli cells (SC), SCs of piglets were treated with sodium nitroprusside (SNP). Changes in cell viability, anti-oxidant activity, enzyme activity and p38 mutagen-activated protein kinase (p38MAPK) activation were detected. The results were as follows. A low concentration of NO can keep SC microtubule and cell viability normal, and a high concentration of NO could increase p38MAPK activation, decrease anti-oxidant activity and transferrin secretion, and destroy the structure and distribution of the microtubules. The results suggest that SNP treatment results in an increase in NO in SCs and decreased cell anti-oxidant activity. The high concentration of NO destroys cell microtubules by activating p38MAPK.


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