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• W2143466853 abstract "The lumen of the inner ear has an unusually low concentration of endolymphatic Na + , which is important for transduction processes. We have recently shown that glucocorticoid receptors (GR) stimulate absorption of Na + 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 + 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 α-, β-, and γ-subunits of the epithelial sodium channel (ENaC); the α 1 -, α 3 -, β 1 -, and β 3 -isoforms of Na + -K + -ATPase; inwardly rectifying potassium channels [IC 50 of short circuit current ( I sc ) for Ba 2+ : 210 μM] 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); 11β-hydroxysteroid dehydrogenase (11β-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 α 4 -subunit of Na + -K + -ATPase, Kir1.1, Kir3.2, Kir3.4, Kir6.1, Kir6.2, and SUR2 were found to be absent, and I sc was not inhibited by glibenclamide. Dexamethasone (100 nM for 24 h) not only upregulated the transcript expression of α-ENaC (∼4-fold), β 2 -subunit (∼2-fold) and β 3 -subunit (∼8-fold) of Na + -K + -ATPase, Kir2.1 (∼5-fold), Kir2.2 (∼9-fold), Kir2.4 (∼3-fold), Kir3.1 (∼ 3- fold), Kir3.3 (∼2-fold), Kir4.2 (∼3-fold ), Kir7.1 (∼2-fold), Sgk1 (∼4-fold), and Nedd4-2 (∼2-fold) but also downregulated GR (∼3-fold) and 11β-HSD1 (∼2-fold). Expression of GR and 11β-HSD1 was higher than MR and 11β-HSD2 in the absence of dexamethasone. Dexamethasone altered transcript expression levels (α-ENaC and Sgk1) by activation of GR but not MR. Proteins were present for the α-, β-, and γ-subunits of ENaC and Sgk1, and expression of α- and γ-ENaC was upregulated by dexamethasone. These findings are consistent with the genomic stimulation by glucocorticoids of Na + absorption by SCCD and provide an understanding of the therapeutic action of glucocorticoids in the treatment of Meniere's disease." @default.
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• W2143466853 date "2006-02-01" @default.
• W2143466853 modified "2023-10-18" @default.
• W2143466853 title "Glucocorticoid regulation of genes in the amiloride-sensitive sodium transport pathway by semicircular canal duct epithelium of neonatal rat" @default.
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• W2143466853 doi "https://doi.org/10.1152/physiolgenomics.00006.2005" @default.
• W2143466853 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16263802" @default.
• W2143466853 hasPublicationYear "2006" @default.
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