No Effect of Dexamethasone on Dex-Rasl mRNA Human Embryonic Kidney (HEK 293) Cells

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.