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J Biol Chem, Vol. 274, Issue 24, 16973-16978, June 11, 1999
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From the The early phase of the stimulatory effect of
aldosterone on sodium reabsorption in renal epithelia is thought to
involve activation of apical sodium channels. However, the genes
initiating this effect are unknown. We used a combination of polymerase
chain reaction-based subtractive hybridization and differential display techniques to identify aldosterone-regulated immediate early genes in
renal mineralocorticoid target cells. We report here that aldosterone rapidly increases mRNA levels of a putative Ser/Thr kinase,
sgk (or serum- and
glucocorticoid-regulated kinase), in its native target cells, i.e. in cortical collecting duct cells. The
effect occurs within 30 min of the addition of aldosterone, is mediated through mineralocorticoid receptors, and does not require de
novo protein synthesis. The full-length sequences of rabbit and
mouse sgk cDNAs were determined. Both cDNAs show
significant homology to rat and human sgk (88-94% at the
nucleotide level, and 96-99% at the amino acid level). Coexpression
of the mouse sgk in Xenopus oocytes with the
three subunits of the epithelial Na+ channel results in a
significantly enhanced Na+ current. These results suggest
that sgk is an immediate early aldosterone-induced gene,
and this protein kinase plays an important role in the early phase of
aldosterone-stimulated Na+ transport.
Department of Physiology, Dartmouth Medical
School, Lebanon, New Hampshire 03756-0001 and ¶ Department of
Cellular and Molecular Physiology, School of Medicine, Yale University,
New Haven, Connecticut 06520
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Q. Tong, R. E. Booth, R. T. Worrell, and J. D. Stockand Regulation of Na+ transport by aldostero |
