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Transcription profiling of cortical collecting duct/connecting nephron tissue from mice treated with aldosterone, canrenoate vs. controls to identify gene products regulated by aldosterone in target cells

ABSTRACT: The mineralocorticoid hormone aldosterone controls sodium reabsorption and blood pressure largely by regulating the cell-surface expression and function of the epithelial sodium channel ENaC in target kidney tubules. Part of the stimulatory effect of aldosterone on ENaC is mediated by the induction of SGK1, a kinase that interferes with the ubiquitylation of ENaC by ubiquitin-protein ligase Nedd4-2. We performed a microarray study in order to investigate which other gene products are rapidly regulated by aldosterone in target cells that participate to the control of Na+ reabsorption and K+ secretion.

ORGANISM(S): Mus musculus

SUBMITTER: Panagiotis Fakitsas

PROVIDER: E-TABM-229 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Early aldosterone-induced gene product regulates the epithelial sodium channel by deubiquitylation.

Fakitsas Panagiotis P Adam Gabriele G Daidié Dorothée D van Bemmelen Miguel X MX Fouladkou Fatemeh F Patrignani Andrea A Wagner Ulrich U Warth Richard R Camargo Simone M R SM Staub Olivier O Verrey François F

Journal of the American Society of Nephrology : JASN 20070307 4

The mineralocorticoid hormone aldosterone controls sodium reabsorption and BP largely by regulating the cell-surface expression and function of the epithelial sodium channel (ENaC) in target kidney tubules. Part of the stimulatory effect of aldosterone on ENaC is mediated by the induction of serum- and glucocorticoid-regulated kinase 1 (Sgk1), a kinase that interferes with the ubiquitylation of ENaC by ubiquitin-protein ligase Nedd4-2. In vivo early aldosterone-regulated mRNA now has been identi ...[more]

PMID: 17344426

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Rapid Aldosterone Effects in Mouse Kidney Distal Convoluted Tubules Cells

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Effect of 48 h aldosterone treatment on late-gestation fetal lung

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Transcription profiling of mouse inner medullary collecting duct cells treated with aldosterone to characterize early aldosterone-responsive genes.

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Project description:The sodium chloride cotransporters (NCC) and the epithelial sodium channel (ENaC) have been reported to be the main effectors of aldosterone in Na+ and Cl- reabsorption in the distal nephron and dietary K+ downregulates NCC. The Cl-/HCO3- exchanger pendrin has been revealed as a key role in maintaining extracellular fluid and electrolyte homeostasis by regulating Cl- reabsorption in the aldosterone-sensitive distal nephron working in tandem with ENaC and perhaps NCC. Pendrin-mediated Cl-/HCO3- exchange is stimulated in models of metabolic alkalosis (e.g. aldosterone administration or dietary NaHCO3 intake), and plasma K+ level is thought to negatively influence pendrin. In this study we used high-throughput proteomics and bioinformatics approaches to analyze urinary exosome contents isolated from patients undergoing fludrocortisone suppression test (FST, as a means of confirming or excluding primary aldosteronism [PA]) to examine the actions of administration of aldosterone analogs, NaCl and KCl orally on transmembrane proteins existing in urinary exosomes.

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Transmembrane serine protease 2 and proteolytic activation of the epithelial sodium channel in mouse kidney: Early effects of aldosterone

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