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Articles in PresS, published online ahead of print October 30, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00159.2001
Submitted on May 18, 2001
Accepted on October 23, 2001
1 Institute of Physiology, University of Wurzburg, Wurzburg, Germany
* To whom correspondence should be addressed. E-mail: michael.gekle{at}mail.uni-wuerzburg.de.
Epidermal growth factor (EGF) regulates cell proliferation, differentiation and ion transport using ERK1/2 as downstream signal. Furthermore, the EGF-receptor (EGF-R) is involved in signaling by G-protein-coupled receptors, growth hormone and cytokines via transactivation. It has been suggested that steroids interact with peptide hormones in part by rapid, potentially non-genomic, mechanisms. Previously, we have shown that aldosterone modulates Na+/H+-exchange in Madin-Darby canine kidney (MDCK) cells via ERK1/2 in a similar way as compared to growth factors. Here, we tested the hypothesis that aldosterone uses the EGF-R as heterologous signal transducer in MDCK cells. Nanomolar concentrations of aldosterone induce a rapid increase of ERK1/2 phosphorylation, cellular Ca2+-concentration and Na+/H+-exchange activity of similar extent as compared to EGF. Furthermore, aldosterone induced a rapid increase of EGF-R Tyr-phosphorylation and inhibition of EGF-R kinase abolished aldosterone-induced signaling. Inhibition of ERK1/2 phosphorylation reduced the Ca2+ response, whereas prevention of Ca2+-influx did not abolish ERK1/2 phosphorylation. Our data show that aldosterone uses the EGF-R-ERK1/2 signaling cascade to elicit its rapid effects in MDCK cells.
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