Cited by 65Ion Transport and Channel RegulationIon channel regulation and functionRenin-Angiotensin System Studies

Hypotonic induction of SGK1 and Na+transport in A6 cells

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Rozansky, David J., Wang, Jian, Doan, Ninh, Purdy, Timothy, Faulk, Tonya, Bhargava, Aditi, Dawson, Kevin, Pearce, David·2002·American Journal of Physiology-Renal Physiology

Abstract

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-mediated transepithelial Na+ transport. In other tissues, including liver and shark rectal gland, SGK1 is regulated by hypertonic stress and is thought to modulate epithelial Na+ channel- and Na+-K+-2Cl- cotransporter-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 line 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 pretreated with an inhibitor of phosphatidylinositol 3-kinase (PI3K), Na+ transport was blunted and only inactive forms of SGK1 were expressed. Surprisingly, these results demonstrate that both hypertonic 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 vo…

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Crossref · 10.1152/ajprenal.00176.2001

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Authors
Rozansky, D. J., Wang, J., Doan, N., Purdy, T., Faulk, T., Bhargava, A., Dawson, K., & Pearce, D.
Affiliations
  • Division of Nephrology, Department of Pediatrics, and
  • University of California, San Francisco (US)
  • Oregon Health & Science University (US)
Venue
American Journal of Physiology-Renal Physiology
Published
2002-07-01
Volume
283
Issue
1
Pages
F105-F113
ISSN
  • 1522-1466 (ISSN-L)
  • 1931-857X
OpenAlex
W2115774544
Cited by
65
References
0
Citations by year
2024: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 1
FWCI
2.43
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • American Journal of Physiology-Renal Physiology (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK 56695, R01-DK-51151, R01DK051151, R01DK056695)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Keywords
SGK1, hypotonic stress, osmotic stress, sodium transport, A6 cells, distal nephron, epithelial Na+ channel, Na+-K+-2Cl- cotransporter, PI3K signaling, gene expression regulation, cell type-specific responses, extracellular volume, Xenopus laevis
MeSH terms
Phosphoinositide-3 Kinase Inhibitors, Serum-Glucocorticoid Regulated Kinases, Animals, Cell Line, Chromones, Enzyme Inhibitors, Hypertonic Solutions, Hypotonic Solutions, Morpholines, Nuclear Proteins, Osmotic Pressure, RNA, Messenger, Sodium, Transcription, Genetic, Water-Electrolyte Balance, Sodium Channels, Gene Expression Regulation, Enzymologic, Protein Serine-Threonine Kinases, Immediate-Early Proteins, Epithelial Sodium Channels

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