Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone.

The renal handling of salt and protons and bicarbonate are intricately linked through shared transport mechanisms for sodium, chloride, protons, and bicarbonate. In the collecting duct, the regulated fine-tuning of salt and acid-base homeostasis is achieved by a series of transport proteins located...

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Main Authors: Nilufar Mohebbi, Angelica Perna, Jenny van der Wijst, Helen M Becker, Giovambattista Capasso, Carsten A Wagner
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3561381?pdf=render
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author Nilufar Mohebbi
Angelica Perna
Jenny van der Wijst
Helen M Becker
Giovambattista Capasso
Carsten A Wagner
author_facet Nilufar Mohebbi
Angelica Perna
Jenny van der Wijst
Helen M Becker
Giovambattista Capasso
Carsten A Wagner
author_sort Nilufar Mohebbi
collection DOAJ
description The renal handling of salt and protons and bicarbonate are intricately linked through shared transport mechanisms for sodium, chloride, protons, and bicarbonate. In the collecting duct, the regulated fine-tuning of salt and acid-base homeostasis is achieved by a series of transport proteins located in different cell types, intercalated and principal cells. Intercalated cells are considered to be of less importance for salt handling but recent evidence has suggested that the anion exchanger pendrin may participate in salt reabsorption and blood pressure regulation. Here, we examined the regulated expression of two functionally related but differentially expressed anion exchangers, AE1 and pendrin, by dietary electrolyte intake and aldosterone. Cortical expression of pendrin was regulated on mRNA and protein level. The combination of NaHCO₃ and DOCA enhanced pendrin mRNA and protein levels, whereas DOCA or NaHCO₃ alone had no effect. NaCl or KHCO₃ increased pendrin mRNA, KCl decreased its mRNA abundance. On protein level, NH₄Cl, NaCl, and KCl reduced pendrin expression, the other treatments were without effect. In contrast, AE1 mRNA or protein expression in kidney cortex was regulated by none of these treatments. In kidney medulla, NaHCO₃/DOCA or NaHCO₃ alone enhanced AE1 mRNA levels. AE1 protein abundance was increased by NH₄Cl, NaHCO₃/DOCA, and NaCl. Immunolocalization showed that during NH₄Cl treatment the relative number of AE1 positive cells was increased and pendrin expressing cells reduced. Thus, pendrin and AE1 are differentially regulated with distinct mechanisms that separately affect mRNA and protein levels. Pendrin is regulated by acidosis and chloride intake, whereas AE1 is enhanced by acidosis, NaCl, and the combination of DOCA and NaHCO₃.
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spelling doaj.art-96e1db0f29fb4ce48539755622defa982022-12-22T00:20:54ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0181e5528610.1371/journal.pone.0055286Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone.Nilufar MohebbiAngelica PernaJenny van der WijstHelen M BeckerGiovambattista CapassoCarsten A WagnerThe renal handling of salt and protons and bicarbonate are intricately linked through shared transport mechanisms for sodium, chloride, protons, and bicarbonate. In the collecting duct, the regulated fine-tuning of salt and acid-base homeostasis is achieved by a series of transport proteins located in different cell types, intercalated and principal cells. Intercalated cells are considered to be of less importance for salt handling but recent evidence has suggested that the anion exchanger pendrin may participate in salt reabsorption and blood pressure regulation. Here, we examined the regulated expression of two functionally related but differentially expressed anion exchangers, AE1 and pendrin, by dietary electrolyte intake and aldosterone. Cortical expression of pendrin was regulated on mRNA and protein level. The combination of NaHCO₃ and DOCA enhanced pendrin mRNA and protein levels, whereas DOCA or NaHCO₃ alone had no effect. NaCl or KHCO₃ increased pendrin mRNA, KCl decreased its mRNA abundance. On protein level, NH₄Cl, NaCl, and KCl reduced pendrin expression, the other treatments were without effect. In contrast, AE1 mRNA or protein expression in kidney cortex was regulated by none of these treatments. In kidney medulla, NaHCO₃/DOCA or NaHCO₃ alone enhanced AE1 mRNA levels. AE1 protein abundance was increased by NH₄Cl, NaHCO₃/DOCA, and NaCl. Immunolocalization showed that during NH₄Cl treatment the relative number of AE1 positive cells was increased and pendrin expressing cells reduced. Thus, pendrin and AE1 are differentially regulated with distinct mechanisms that separately affect mRNA and protein levels. Pendrin is regulated by acidosis and chloride intake, whereas AE1 is enhanced by acidosis, NaCl, and the combination of DOCA and NaHCO₃.http://europepmc.org/articles/PMC3561381?pdf=render
spellingShingle Nilufar Mohebbi
Angelica Perna
Jenny van der Wijst
Helen M Becker
Giovambattista Capasso
Carsten A Wagner
Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone.
PLoS ONE
title Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone.
title_full Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone.
title_fullStr Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone.
title_full_unstemmed Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone.
title_short Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone.
title_sort regulation of two renal chloride transporters ae1 and pendrin by electrolytes and aldosterone
url http://europepmc.org/articles/PMC3561381?pdf=render
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AT jennyvanderwijst regulationoftworenalchloridetransportersae1andpendrinbyelectrolytesandaldosterone
AT helenmbecker regulationoftworenalchloridetransportersae1andpendrinbyelectrolytesandaldosterone
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