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Receptor tyrosine kinases‐mediated mechanism in hypotonicity‐provoked Na + reabsorption in renal epithelial A6 cells
Author(s) -
Taruno Akiyuki,
Niisato Naomi,
Marunaka Yoshinori
Publication year - 2006
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.20.4.a346-c
Subject(s) - reabsorption , epithelial sodium channel , amiloride , tonicity , tyrosine kinase , chromosomal translocation , chemistry , receptor tyrosine kinase , medicine , microbiology and biotechnology , signal transduction , endocrinology , receptor , phosphorylation , ion transporter , kinase , biology , kidney , biochemistry , sodium , organic chemistry , membrane , gene
In the amphibian kidney epithelium, A6, hypotonicity increases transepithelial Na + transport via translocation of intracellular epithelial Na + channel (ENaC) to the apical surface in a protein tyrosine kinase (PTK)‐dependent manner. Evaluating effects of inhibitors on hypotonicity‐induced amiloride‐sensitive short‐circuit current and conductance to determine what type of PTK is involved in hypotonic action, we identified that receptor tyrosine kinases (RTKs) were involved in the stimulatory action of hypotonic stress on ENaC translocation. Further, we found that the downstream of this RTKs‐mediated signaling pathway was not mediated via PI3 kinase‐SGK1 signaling pathway, which participates in hypotonicity‐induced ENaC translocation. Interestingly, our experimental data also disclosed that these two hypotonicity‐activated signaling pathways had the completely different effects on hypotonicity‐induced Na + reabsorption. In addition to the above, we found an interesting possibility that JNK was located in the downstream of hypotonicity‐activated RTKs to activation of ENaC translocation. These data supports the concept of novel RTKs‐mediated mechanism in Na + reabsorption in response to the hypo‐osmotic stress. Supported by Grants‐in‐Aids from JSPS (17390057 and 17590191).