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Articles in PresS, published online ahead of print February 19, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00176.2001
Submitted on June 6, 2001
Accepted on February 7, 2002
1 Pediatrics, UCSF, San Francisco, CA, USA
2 Medicine, UCSF, San Francisco, CA, USA
3 Pediatrics, Oregon Health & Science University, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: pearce{at}cgl.ucsf.edu.
Serum and glucocorticoid-regulated kinase-1 (SGK1) is a serine-threonine kinase that is regulated at the transcriptional level by numerous regulatory inputs, including mineralocorticoids, glucocorticoids, follicle stimulating hormone, and osmotic stress. In the distal nephron, SGK1 is induced by aldosterone and regulates epithelial Na+ channel (ENaC)- mediated transepithelial Na+ transport. In other tissues, including liver and shark rectal gland, SGK1 is regulated by hypertonic stress where it is thought to modulate ENaC and Na+-K+-2Cl- cotransporter (NKCC)-mediated Na+ transport. In this report, we examined the regulation of SGK1 mRNA and protein expression and Na+ currents in response to osmotic stress in A6 cells, a cultured cell derived from Xenopus laevis distal nephron. We found that, in contrast to hepatocytes and rectal gland cells, hypotonic conditions stimulated SGK1 expression and Na+ transport in A6 cells. Moreover, a correlation was found between SGK1 induction and the later phase of activation of Na+ transport in response to hypotonic treatment. When A6 cells were pre-treated with an inhibitor of phosphatidylinositol 3-kinase (PI3K), Na+ transport was blunted and only inactive forms of SGK1 were expressed. These results demonstrate, surprisingly, that both hyper- and hypotonic stimuli can induce SGK1 gene expression in a cell type dependent fashion. Moreover, these data lend support to the view that SGK1 contributes to the defense of extracellular fluid volume and tonicity in amphibia by mediating a component of the hypotonic induction of distal nephron Na+ transport.
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