scholarly journals Follicle-Stimulating Hormone Induction of Steel Factor (SLF) mRNA in Mouse Sertoli Cells and Stimulation of DNA Synthesis in Spermatogonia by Soluble SLF

1993 ◽  
Vol 155 (1) ◽  
pp. 68-74 ◽  
Author(s):  
Pellegrino Rossi ◽  
Susanna Dolci ◽  
Cristina Albanesi ◽  
Paola Grimaldi ◽  
Rossana Ricca ◽  
...  
1978 ◽  
Vol 56 (9) ◽  
pp. 875-879 ◽  
Author(s):  
Irving B. Fritz ◽  
Michael D. Griswold ◽  
B. Gregory Louis ◽  
Jennifer H. Dorrington

The concentration of cholera toxin required for half-maximal stimulation of cAMP production by Sertoli cell enriched cultures (4.48 × 10−2 μg/ml) is greater than that required for half-maximal stimulation of 17β-estradiol synthesis from testosterone (2.34 × 10−4 μg/ml), [3H]thymidine incorporation into DNA (1.48 × 10−5μg/ml), or androgen binding protein production (2.43 × 10−6 μg/ml). The same relative dose response hierarchy was obtained with respect to stimulation of Sertoli cells with follicle stimulating hormone (FSH) preparations. Again, highest concentrations were required to elicit maximal cAMP production. The data are discussed in relation to an apparent paradox: If cAMP is the mediating 'second messenger' following stimulation by FSH or cholera toxin, why should highest concentrations of these agents be required to elicit 50% of maximal cAMP levels?


Author(s):  
O. N Nwankudu

Follicle Stimulating Hormone (FSH) is a polypeptide hormone secreted by the cells of the anterior pituitary whose primary function is stimulation of ovarian follicle to grow and mature in females. Additionally, FSH stimulates the granulosa cells in the ovarian follicle to synthesize aromatase which converts androgen produced by the thecal cells to estradiol. Estradiol in the blood primes the hypothalamus to produce stronger pulses of Gonadotropin Releasing Hormone (GnRH) leading to secretion of Luteinizing hormone (LH). Then, LH causes ovulation and the developmentof corpus luteum. But, in the males, FSH stimulates the Sertoli cells to secret Androgen Binding Protein (ABP) which concentrates local testosterone leading to stimulation of spermatogenesis. However, FSH has been identified in many angiogenic vasculature of many tumors. The review tries to bring out FSH in reproduction and pathology as well as reveal certain solutions which may be useful in infertility and oncogenic therapy.


Zygote ◽  
1994 ◽  
Vol 2 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Zai Si Ji ◽  
Shin-Ichi Abeé

SummaryWe previously showed in organ culture of testes fragments from Cynops pyrrhogaster that mammalian folicle-stimulating hormone (FSH) stimulates secondary spermatogonia to differentiate into primary spermatocytes. In this report, we demonstrate in organ culture that FSH stimulates DNA synthesis in secondary spermatogonia and Sertoli cells: the numbers of secondary spermatogonia and Sertoli cells incorporating 5-bromo-2′ -deoxyuridine (BrdU)throughout the culture period in the presence of FSH were 3-5 times those incorporating BrdU in the absence of FSH. Moreover, addition of FSH, induced after a day a remarkable increase in the number of spermatogonia and Sertoli cells incorporating BrdU. The above results indicate that FSH stimulates and induces DNA synthesis in spermatogonia and Sertoli cells. Most of the spermatogonia within a cyst were labelled simultaneously and at the same density, indicating that they underwent synchronous DNA synthesis, whereas all the Sertoli cells within a cyst were not labelled simultaneously, indicating that they synthesised DNA asynchronously. When testes fragments pulse-labelled with Brdu were cultured in FSH for 14 days, the secondary spermatogonia differentiated into primary spermatocytes, whereas in the absence of FSH they failed to differentiate and most died by the 7th day. The above results together show that FSH is required for the proliferation of both secondary spermatogonia and Sertoli cells as well as the differentiation of secondary spermatogonia into primary spermatocytes.


1991 ◽  
Vol 125 (3) ◽  
pp. 280-285 ◽  
Author(s):  
J. Alan Talbot ◽  
Ann Lambert ◽  
Robert Mitchell ◽  
Marek Grabinski ◽  
David C. Anderson ◽  
...  

Abstract We have investigated the role of Ca2+ in the control of FSH-induced estradiol secretion by Sertoli cells isolated from 8-10 days old rats. Exogenous Ca2+ (4-8 mmol/1) inhibited FSH-stimulated E2 secretion such that, with 8 mmol/l Ca2+ and FSH (8 IU/l) E2 secretion decreased from 2091±322 to 1480±84 pmol/l (p<0.002), whilst chelation of Ca2+ in the culture medium with EGTA (3 mmol/l) increased E2 secretion from 360±45 to 1242±133 pmol/l) in the absence of FSH. Further, EGTA (3 mmol/l) markedly potentiated FSH (8 IU/l), forskolin (1 μmol/l) and dibutyryl cAMP (1 mmol/l)-stimulated E2 secretion. Addition of the Ca2+ ionophores, ionomycin (2-5 μmol/l) and A23187 (2 μmol/l), inhibited FSH (8 IU/l)-stimulated E2 secretion by >80%. The effect of ionomycin was totally reversible, whereas that of A23187 was irreversible. Ionomycin (5 μmol/l) had no effect on EGTA-induced E2 secretion in the absence of FSH, but reduced EGTA-provoked E2 secretion by 59% in the presence of FSH (8 IU/l). Similarly, forskolin- and dibutyryl cAMP-provoked E2 production was inhibited 46-50% by ionomycin (5 μmol/l). We conclude that FSH-induced E2 secretion from immature rat Sertoli cells is modulated by intra- and extracellular Ca2+.


Sign in / Sign up

Export Citation Format

Share Document