{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T05:23:44Z","timestamp":1791177824334,"version":"4.1.0"},"reference-count":63,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiological Genomics"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:p>The lumen of the inner ear has an unusually low concentration of endolymphatic Na<jats:sup>+<\/jats:sup>, which is important for transduction processes. We have recently shown that glucocorticoid receptors (GR) stimulate absorption of Na<jats:sup>+<\/jats:sup>by semicircular canal duct (SCCD) epithelia. In the present study, we sought to determine the presence of genes involved in the control of the amiloride-sensitive Na<jats:sup>+<\/jats:sup>transport pathway in rat SCCD epithelia and whether their level of expression was regulated by glucocorticoids using quantitative real-time RT-PCR. Transcripts were present for \u03b1-, \u03b2-, and \u03b3-subunits of the epithelial sodium channel (ENaC); the \u03b1<jats:sub>1<\/jats:sub>-, \u03b1<jats:sub>3<\/jats:sub>-, \u03b2<jats:sub>1<\/jats:sub>-, and \u03b2<jats:sub>3<\/jats:sub>-isoforms of Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase; inwardly rectifying potassium channels [IC<jats:sub>50<\/jats:sub>of short circuit current ( I<jats:sub>sc<\/jats:sub>) for Ba<jats:sup>2+<\/jats:sup>: 210 \u03bcM] Kir2.1, Kir2.2, Kir2.3, Kir2.4, Kir3.1, Kir3.3, Kir4.1, Kir4.2, Kir5.1, and Kir7.1; sulfonyl urea receptor 1 (SUR1); GR; mineralocorticoid receptor (MR); 11\u03b2-hydroxysteroid dehydrogenase (11\u03b2-HSD) types 1 and 2; serum- and glucocorticoid-regulated kinase 1 (Sgk1); and neural precursor cell-expressed developmentally downregulated 4-2 (Nedd4-2). On the other hand, transcripts for the \u03b1<jats:sub>4<\/jats:sub>-subunit of Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase, Kir1.1, Kir3.2, Kir3.4, Kir6.1, Kir6.2, and SUR2 were found to be absent, and I<jats:sub>sc<\/jats:sub>was not inhibited by glibenclamide. Dexamethasone (100 nM for 24 h) not only upregulated the transcript expression of \u03b1-ENaC (\u223c4-fold), \u03b2<jats:sub>2<\/jats:sub>-subunit (\u223c2-fold) and \u03b2<jats:sub>3<\/jats:sub>-subunit (\u223c8-fold) of Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase, Kir2.1 (\u223c5-fold), Kir2.2 (\u223c9-fold), Kir2.4 (\u223c3-fold), Kir3.1 (\u223c 3- fold), Kir3.3 (\u223c2-fold), Kir4.2 (\u223c3-fold ), Kir7.1 (\u223c2-fold), Sgk1 (\u223c4-fold), and Nedd4-2 (\u223c2-fold) but also downregulated GR (\u223c3-fold) and 11\u03b2-HSD1 (\u223c2-fold). Expression of GR and 11\u03b2-HSD1 was higher than MR and 11\u03b2-HSD2 in the absence of dexamethasone. Dexamethasone altered transcript expression levels (\u03b1-ENaC and Sgk1) by activation of GR but not MR. Proteins were present for the \u03b1-, \u03b2-, and \u03b3-subunits of ENaC and Sgk1, and expression of \u03b1- and \u03b3-ENaC was upregulated by dexamethasone. These findings are consistent with the genomic stimulation by glucocorticoids of Na<jats:sup>+<\/jats:sup>absorption by SCCD and provide an understanding of the therapeutic action of glucocorticoids in the treatment of Meniere's disease.<\/jats:p>","DOI":"10.1152\/physiolgenomics.00006.2005","type":"journal-article","created":{"date-parts":[[2005,11,2]],"date-time":"2005-11-02T01:24:53Z","timestamp":1130894693000},"page":"114-123","source":"Crossref","is-referenced-by-count":54,"title":["Glucocorticoid regulation of genes in the amiloride-sensitive sodium transport pathway by semicircular canal duct epithelium of neonatal rat"],"prefix":"10.1152","volume":"24","author":[{"given":"Satyanarayana R.","family":"Pondugula","sequence":"first","affiliation":[{"name":"Cellular Biophysics Laboratory, Department of Anatomy and Physiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nithya N.","family":"Raveendran","sequence":"additional","affiliation":[{"name":"Cellular Biophysics Laboratory, Department of Anatomy and Physiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zuhal","family":"Ergonul","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youping","family":"Deng","sequence":"additional","affiliation":[{"name":"Division of Biology, Bioinformatics Center, Kansas State University, Manhattan, Kansas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Chen","sequence":"additional","affiliation":[{"name":"Division of Biology, Bioinformatics Center, Kansas State University, Manhattan, Kansas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel D.","family":"Sanneman","sequence":"additional","affiliation":[{"name":"Cellular Biophysics Laboratory, Department of Anatomy and Physiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lawrence G.","family":"Palmer","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel C.","family":"Marcus","sequence":"additional","affiliation":[{"name":"Cellular Biophysics Laboratory, Department of Anatomy and Physiology"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.62.1.573"},{"key":"R1A","doi-asserted-by":"crossref","unstructured":"Alvareze de la Rosa D, Gimenez I, Forbush B, and Canessa CM.SGK1 activates Na+-K+-ATPase in amphibian renal epithelial cells.Am J Physiol Cell Physiol. 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