مرکز منطقه ای اطلاع رساني علوم و فناوري -

چكيده لاتين :

Previous work has indicated that dex-rasl is a glucocorticoid-induced protein that could mediate the effects of adrenal corticosteroids on the secretion of adrenocorticotrophic hormone. In the present study the effect of the synthetic gluocorticoid dexamethasone on dex-rasl expression was examined in HEK293 cells. A GR-reporter construct in which the expression of luciferase is under the control of the mammary tumor virus long-term repeat segment was transiently transfected into HEK 293 cells. The cells were exposed to dexamethasone 48h later. Analysis of dexamethasone action revealed dose- and time-dependent induction of luciferase activity. Analysis of the expression of endogenous mRNAs revealed expression of a ~5kb dex-rasl and a ~2.6kb glucocorticoid-induced protein kinase (SGK-1) mRNA species in HEK 293 cells. Dexamethasone had no significant effect on Dex-rasl mRNA following varying times of treatment (0 to 120 min) but significantly increased SGK-1 mRNA with maximum effect at 30 min. The results suggest that in HEK 293 cells; 1) dexamethasone acts via endogenously expressed GR; 2) Dex-rasl is not a glucocorticoid-induced gene in this system, while SGK-1 mRNA is induced.