Somatostatin inhibits stem cell factor messenger RNA expression by Sertolicells and stem cell factor-induced DNA synthesis in isolated seminiferous tubules

Citation
I. Goddard et al., Somatostatin inhibits stem cell factor messenger RNA expression by Sertolicells and stem cell factor-induced DNA synthesis in isolated seminiferous tubules, BIOL REPROD, 65(6), 2001, pp. 1732-1742
Citations number
48
Categorie Soggetti
da verificare
Journal title
BIOLOGY OF REPRODUCTION
ISSN journal
00063363 → ACNP
Volume
65
Issue
6
Year of publication
2001
Pages
1732 - 1742
Database
ISI
SICI code
0006-3363(200112)65:6<1732:SISCFM>2.0.ZU;2-R
Abstract
Immature porcine Sertoli cells have been reported to be targets for the reg ulatory peptide somatostatin (SRIF), which inhibits the basal and FSH-induc ed proliferation of Sertoli cells through a decrease of cAMP production. in the present study, we show that SRIF inhibits both basal and FSH-stimulate d expression of the stem cell factor (SCF), a Sertoli cell-specific gene. T he SRIF-mediated inhibition of forskolin-triggered, but not of 8-bromoadeno sine-cAMP-triggered, SCF mRNA expression demonstrates the involvement of ad enylyl cyclase in underlying peptide actions. Moreover, these effects requi re functional coupling of specific plasma membrane receptors to adenylyl cy clase via inhibitory G proteins, because pertussis toxin prevents SRIF-medi ated inhibition of SCF mRNA expression. Reverse transcription-polymerase ch ain reaction (RT-PCR) and Western blot assays suggest the involvement of ss t2 receptors in SRIF actions on Sertoli cells. The biological relevance of these data is supported by an SRIF-mediated decrease in SCF-induced incorpo ration of [H-3]thymidine in isolated seminiferous tubules. In situ hybridiz ation and confocal microscopy show that, in seminiferous tubules only, sper matogonia display both c-kit and sst2 receptors. Taken together, these resu lts suggest that SCF-stimulated DNA synthesis can be inhibited by SRIF in s permatogonia, but not in Sertoli and peritubular cells. Combined RT-PCR and immunohistochemical approaches point toward spermatogonia and Leydig cells as the source of testicular SRIF. These data argue in favor of paracrine/a utocrine SRIF actions in testis.