| First Author | Riaz H | Year | 2013 |
| Journal | J Steroid Biochem Mol Biol | Volume | 138 |
| Pages | 257-66 | PubMed ID | 23831358 |
| Mgi Jnum | J:205072 | Mgi Id | MGI:5543980 |
| Doi | 10.1016/j.jsbmb.2013.06.007 | Citation | Riaz H, et al. (2013) Somatostatin and its receptors: functional regulation in the development of mice Sertoli cells. J Steroid Biochem Mol Biol 138:257-66 |
| abstractText | Recently, Sertoli cells have been ascertained as the target for the regulatory peptide somatostatin (SST). Therefore, the present study investigated the expression of somatostatin receptors, their age-related alterations and homologous regulation by in vitro treatment with SRIF14 on mice Sertoli cells; furthermore, it dealt with SRIF14 action on growth progression, apoptotic activity and related gene expressions in these cells. We found that mice Sertoli cells expressed all SST1-5 receptors with differential intensities. Age-related real-time PCR of all somatostatin receptors identified abundance of SSTR2 and SSTR5 mRNA level during Sertoli cell developmental period. Furthermore, higher level of these two receptors was independent of SRIF14, as treatment with SRIF14 failed to induce both receptor expressions when compared with control. Somatostatin treatment elicited a dose-dependent decrease in forskolin stimulated cAMP production. Low (100pM and 10nM) and high dosage (1muM) groups of SRIF14 significantly promoted apoptosis, while all treatment groups led to dose dependent cessation (P<0.05) of G1 phase of cell cycle as further validated by increase in casp3, decrease in bcl2, elevation of P21 (all by western blot) and decrease in Igf1 expressions, similarly, SST treatment caused a dose dependent suppression in the mRNA level of kitl gene, which is important in the regulation of spermatogenesis. These findings suggest that somatostatin and its receptors (SSTR2 and SSTR5) are important markers in the regulation and development of Sertoli cell; furthermore, it portrays physiological inhibitory role in Sertoli cell development by inducing apoptosis and cell cycle arrest. |
