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Am J Physiol Renal Physiol (November 9, 2004). doi:10.1152/ajprenal.00242.2004
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Submitted on June 29, 2004
Accepted on November 7, 2004

Gene Regulation of ENaC subunits by Serum and Glucocorticoid Inducible Kinase-1 (SGK1)

Cary Boyd1 and Aniko Naray-Fejes-Toth1*

1 Department of Physiology, Dartmouth Medical School, Lebanon, NH, 03756-0001, USA

* To whom correspondence should be addressed. E-mail: Aniko.Fejes-Toth{at}Dartmouth.EDU.

Aldosterone is a key regulator of epithelial Na+ channels (ENaC) in renal cortical collecting ducts (CCD). The goal of this study was to examine whether the serum and glucocorticoid-inducible kinase-1 (SGK1), an aldosterone induced gene, is vital to the delayed effect of aldosterone by increasing the gene expression of ENaC subunits. To test this hypothesis, we compared the levels of ENaC mRNA in mouse CCD cells that stably express either full-length (FL)-SGK1 or a kinase-dead dominant negative (K127M)-SGK1. Our results revealed that SGK1 regulates gene expression of ENaC, whether cells are maintained in steroid-free media (SF), or in the presence of corticosteroids (CS) and/or other growth factors. Under all conditions, the loss of function of SGK1 caused a significant decrease in the expression of {alpha} and {beta}-ENaC, but not {gamma}-ENaC. As compared to cells expressing FL-SGK1, K127M-SGK1 decreased the expression of {alpha}- and {beta}-subunit mRNA by ~45% and ~90%, respectively. Next, to determine if SGK1 is one of the proteins mediating the induction of {alpha}-ENaC mRNA by CS, we compared steroid-induction of {alpha}-ENaC in cells expressing K127M-SGK1 vs. FL-SGK1. The maximum level of {alpha}-ENaC mRNA levels following CS was significantly (~45%) higher in FL-SGK1 vs. K127M-SGK1 expressing cells, although the fold induction by CS was similar in both FL-SGK1 and K127M-SGK1 expressing cells. In summary, we report for the first time that SGK1 regulates transcription of ENaC subunits. We propose that the effect of SGK1 on ENaC transcription is mediated by the activation of unidentified transcription factors.




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