SGK is a primary glucocorticoid-induced gene in the human

Citation
A. Naray-fejes-toth et al., SGK is a primary glucocorticoid-induced gene in the human, J STEROID B, 75(1), 2000, pp. 51-56
Citations number
21
Categorie Soggetti
Biochemistry & Biophysics
Journal title
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
ISSN journal
09600760 → ACNP
Volume
75
Issue
1
Year of publication
2000
Pages
51 - 56
Database
ISI
SICI code
0960-0760(200012)75:1<51:SIAPGG>2.0.ZU;2-M
Abstract
Serum- and glucocorticoid-induced kinase (sgk) is transcriptionally regulat ed by corticosteroids in several cell types. Recent findings suggest that s gk is an important gene in the early action of corticosteroids on epithelia l sodium reabsorption. Surprisingly, the human sgk was reported not to be t ranscriptionally regulated by corticosteroids in a hepatoma cell line, and thus far no glucocorticoid response element has been identified in the huma n SGK gene. Since humans clearly respond to both aldosterone and glucocorti coids in cells where sgk action seems to be important, in this study we det ermined sgk mRNA levels following dexamethasone treatment for various durat ion in five human cell lines. These cell lines included epithelial cells (H 441, T84 and HT29) and lymphoid/monocyte (U937 and THP-1) lines. Using quan titative reverse transcriptase-polymerase chain reaction (RT-PCR), we found that sgk mRNA levels are markedly induced by glucocorticoids in all of the five cell lanes studied. Time course analyses revealed that sgk mRNA level s are elevated as early as 30 min after addition of the glucocorticoid, and remain elevated for several hours. Northern analysis in H441 cells confirm ed that sgk is an early induced gene. The induction of sgk by dexamethasone was unaffected by cycloheximide. indicating that it does not require de no vo protein synthesis. These results indicate that the human sgk, just like its counterparts in other species, is a primary glucocorticoid-induced gene . (C) 2001 Elsevier Science Ltd. All rights reserved.