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Genomic effect of hypotonic stress on Na + reabsorption through Ca 2+ /calmodulin‐dependent SGK1 induction in renal epithelial A6 cells
Author(s) -
Taruno Akiyuki,
Niisato Naomi,
Marunaka Yoshinori
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a954-a
Subject(s) - sgk1 , epithelial sodium channel , ionomycin , reabsorption , bapta , medicine , endocrinology , chemistry , calmodulin , tonicity , calcium , biology , glucocorticoid , kidney , sodium , organic chemistry
Serum‐ and glucocorticoid‐inducible kinase 1 (SGK1) plays a key role in body NaCl homeostasis by fine tuning of renal NaCl reabsorption in the distal nephron via modulation of epithelial Na + channel (ENaC) activity, transcription, and trafficking. Although induction of SGK1 is involved in the stimulatory action of hypotonicity on Na + transport, it is unknown how hypotonicity regulates SGK1 expression. In the present study, we studied if Ca 2+ signal is involved in the hypotonic action on SGK1 expression and Na + transport. Using QRT‐PCR and western blotting, we observed that BAPTA/AM (an intracellular Ca 2+ chelator) and W7 (a calmodulin antagonist) blunted the hypotonic induction of SGK1 mRNA and protein. Ionomycin (a Ca 2+ ionophore) stimulated SGK1 transcription under an isotonic condition. BAPTA/AM retarded the hypotonicity‐induced Na + current. Further, our observation suggests that hypotonicity‐induced expression and activity of SGK1 would be associated with expression of αENaC, but not β or γENaC. Taken together, we conclude that hypotonic stress has genomic action on SGK1 mRNA expression in a Ca 2+ /calmodulin‐dependent manner, stimulating Na + transport and αENaC expression. JSPS17590191, 17390057