Homologous upregulation of gonadotropin-releasing hormone receptor mRNA occurs through transcriptional activation rather than modulation of mRNA stability.

Autor: Cheon, Minseok, Park, Deokbae, Park, Yongbin, Kam, Kyungyoon, Park, Sang, Ryu, Kyungza
Zdroj: Endocrine (1355008X); 2000, Vol. 13 Issue 1, p47-53, 7p
Abstrakt: In a previous study, we showed that even continuous application of gonadotropin-releasing hormone (GnRH) could increase the steady-state levels of GnRH receptor (GnRH-R) mRNA if treated for a relatively short period (6 h). Therefore, in the present study we examined whether GnRH-induced increment of GnRH-R mRNA is owing to stabilization of the preexisting GnRH-R mRNA or new synthesis of GnRH-R mRNA or both. Initially, to examine the effect on new RNA synthesis, the transcription inhibitor, actinomycin D (2 µ M), was added to primary cultured rat anterior pituitary cells. In the presence of transcription inhibitor, GnRH-induced augmentation of GnRH-R mRNA levels was completely abolished. This result indicates that homologous upregulation of GnRH-R mRNA expression occurs at least through new RNA synthesis of GnRH-R gene. We further assessed the effects of GnRH on the turnover rate of GnRH-R mRNA using actinomycin D (2 µ M). The basal half-life of GnRH-R mRNA was estimated to be approx 21 h. The application of GnRH tended to slightly suppress the basal turnover rate of GnRH; however, there was no statistically significant difference, compared with the group treated with actinomycin D alone. Collectively, our results suggest that the homologous upregulation of GnRH-R mRNA may occur through transcriptional activation of GnRH-R gene rather than enhancement of GnRH-R mRNA stability, although we did not examine the transcription rate of GnRH-R gene. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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