In: American Journal of Physiology - Renal Physiology, 2011, vol. 299, no. 6, p. F1473-F1485
Aldosterone and corticosterone bind to mineralocorticoid (MR) and glucocorticoid receptors (GR), which, upon ligand binding, are thought to translocate to the cell nucleus to act as transcription factors. Mineralocorticoid selectivity is achieved by the 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) that inactivates 11β-hydroxy glucocorticoids. High expression levels of 11β-HSD2...
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In: Proceedings of the National Academy of Sciences of the United States of America, 2007, vol. 104, no. 37, p. 14849-14854
The distal convoluted tubule (DCT) plays an essential role in the reabsorption of NaCl by the kidney, a process that can be inhibited by thiazide diuretics. Parvalbumin (PV), a Ca²⁺-binding protein that plays a role in muscle fibers and neurons, is selectively expressed in the DCT, where its role remains unknown. We therefore investigated the renal phenotype of PV knockout mice...
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In: Journal of the American Society of Nephrology, 2005, vol. 16, p. 2279
Aldosterone plays a central role in Na⁺ homeostasis by controlling Na⁺ reabsorption in the aldosterone-sensitive distal nephron involving the epithelial Na⁺ channel (ENaC). Part of the effects of aldosterone is mediated by serum and glucocorticoid-induced kinase 1 (Sgk1), a Ser/Thr kinase whose expression is rapidly induced by aldosterone and that increases in heterologous expression...
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In: Histochemistry and Cell Biology, 2005, vol. 123(4-5), p. 335
Fibrosis is considered as a central factor in the loss of renal function in chronic kidney diseases. The origin of fibroblasts and myofibroblasts that accumulate in the interstitium of the diseased kidney is still a matter of debate. It has been shown that accumulation of myofibroblasts in inflamed and fibrotic kidneys is associated with upregulation of fibroblast-specific protein 1 (FSP1,...
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In: Journal of the American Society of Nephrology, 2006, vol. 17, p. 1264-1274
The activity of the epithelial sodium (Na⁺) channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) needs to be tightly regulated to match urinary Na⁺ excretion with dietary Na⁺ intake. The ubiquitin-protein ligase Nedd4-2, which in vitro interacts with ENaC subunits and reduces ENaC cell surface abundance and activity by ubiquitylation of the channel, may participate in...
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In: Journal of the American Society of Nephrology, 2005, vol. 16, p. 3175
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In: Journal of the American Society of Nephrology, 2005, vol. 16, p. 3642
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In: Journal of Biological Chemistry, 2005, vol. 280, no. 46, p. 38264-38270
Activation of the mitogen-activated protein (MAP) kinase cascade by progesterone in Xenopus oocytes leads to a marked down-regulation of activity of the amiloride-sensitive epithelial sodium channel (ENaC). Here we have studied the signaling pathways involved in progesterone effect on ENaC activity. We demonstrate that: (i) the truncation of the C termini of the αβγENaC subunits...
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In: Journal of the American Society of Nephrology, 2010, vol. 21, p. -
Lithium-induced nephrogenic diabetes insipidus (NDI) is accompanied by polyuria, downregulation of aquaporin 2 (AQP2), and cellular remodeling of the collecting duct (CD). The amiloride-sensitive epithelial sodium channel (ENaC) is a likely candidate for lithium entry. Here, we subjected transgenic mice lacking αENaC specifically in the CD (knockout [KO] mice) and littermate controls to chronic...
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In: The Journal of Clinical Investigation, 2005, vol. 115(6), p. 1651
Thiazide diuretics enhance renal Na⁺ excretion by blocking the Na⁺-Cl⁻ cotransporter (NCC), and mutations in NCC result in Gitelman syndrome. The mechanisms underlying the accompanying hypocalciuria and hypomagnesemia remain debated. Here, we show that enhanced passive Ca²⁺ transport in the proximal tubule rather than active Ca²⁺ transport in distal convolution explains...
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