PortalPublikationenThe AE4 transporter mediates kidney acid-base sensing

The AE4 transporter mediates kidney acid-base sensing

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The AE4 transporter mediates kidney acid-base sensing. / Vitzthum, H; Koch, M; Eckermann, L; Svendsen, S L; Berg, P; Hübner, C A; Leipziger, J; Meyer-Schwesinger, C; Ehmke, H.

in: NAT COMMUN, Jahrgang 14, Nr. 1, 26.05.2023, S. 3051.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Vitzthum, H, Koch, M, Eckermann, L, Svendsen, SL, Berg, P, Hübner, CA, Leipziger, J, Meyer-Schwesinger, C & Ehmke, H 2023, 'The AE4 transporter mediates kidney acid-base sensing', NAT COMMUN, Jg. 14, Nr. 1, S. 3051. https://doi.org/10.1038/s41467-023-38562-x

APA

Vitzthum, H., Koch, M., Eckermann, L., Svendsen, S. L., Berg, P., Hübner, C. A., Leipziger, J., Meyer-Schwesinger, C., & Ehmke, H. (2023). The AE4 transporter mediates kidney acid-base sensing. NAT COMMUN, 14(1), 3051. https://doi.org/10.1038/s41467-023-38562-x

Vancouver

Vitzthum H, Koch M, Eckermann L, Svendsen SL, Berg P, Hübner CA et al. The AE4 transporter mediates kidney acid-base sensing. NAT COMMUN. 2023 Mai 26;14(1):3051. https://doi.org/10.1038/s41467-023-38562-x

Bibtex

@article{ae1f067645d441eea9f0e14357eb9b5b,
title = "The AE4 transporter mediates kidney acid-base sensing",
abstract = "The kidney plays a key role in the correction of systemic acid-base imbalances. Central for this regulation are the intercalated cells in the distal nephron, which secrete acid or base into the urine. How these cells sense acid-base disturbances is a long-standing question. Intercalated cells exclusively express the Na+-dependent Cl-/HCO3- exchanger AE4 (Slc4a9). Here we show that AE4-deficient mice exhibit a major dysregulation of acid-base balance. By combining molecular, imaging, biochemical and integrative approaches, we demonstrate that AE4-deficient mice are unable to sense and appropriately correct metabolic alkalosis and acidosis. Mechanistically, a lack of adaptive base secretion via the Cl-/HCO3- exchanger pendrin (Slc26a4) is the key cellular cause of this derailment. Our findings identify AE4 as an essential part of the renal sensing mechanism for changes in acid-base status.",
keywords = "Mice, Animals, Kidney/metabolism, Membrane Transport Proteins/genetics, Acid-Base Equilibrium/physiology, Nephrons/metabolism, Sulfate Transporters/metabolism, Bicarbonates/metabolism, Chloride-Bicarbonate Antiporters",
author = "H Vitzthum and M Koch and L Eckermann and Svendsen, {S L} and P Berg and H{\"u}bner, {C A} and J Leipziger and C Meyer-Schwesinger and H Ehmke",
note = "{\textcopyright} 2023. The Author(s).",
year = "2023",
month = may,
day = "26",
doi = "10.1038/s41467-023-38562-x",
language = "English",
volume = "14",
pages = "3051",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - The AE4 transporter mediates kidney acid-base sensing

AU - Vitzthum, H

AU - Koch, M

AU - Eckermann, L

AU - Svendsen, S L

AU - Berg, P

AU - Hübner, C A

AU - Leipziger, J

AU - Meyer-Schwesinger, C

AU - Ehmke, H

N1 - © 2023. The Author(s).

PY - 2023/5/26

Y1 - 2023/5/26

N2 - The kidney plays a key role in the correction of systemic acid-base imbalances. Central for this regulation are the intercalated cells in the distal nephron, which secrete acid or base into the urine. How these cells sense acid-base disturbances is a long-standing question. Intercalated cells exclusively express the Na+-dependent Cl-/HCO3- exchanger AE4 (Slc4a9). Here we show that AE4-deficient mice exhibit a major dysregulation of acid-base balance. By combining molecular, imaging, biochemical and integrative approaches, we demonstrate that AE4-deficient mice are unable to sense and appropriately correct metabolic alkalosis and acidosis. Mechanistically, a lack of adaptive base secretion via the Cl-/HCO3- exchanger pendrin (Slc26a4) is the key cellular cause of this derailment. Our findings identify AE4 as an essential part of the renal sensing mechanism for changes in acid-base status.

AB - The kidney plays a key role in the correction of systemic acid-base imbalances. Central for this regulation are the intercalated cells in the distal nephron, which secrete acid or base into the urine. How these cells sense acid-base disturbances is a long-standing question. Intercalated cells exclusively express the Na+-dependent Cl-/HCO3- exchanger AE4 (Slc4a9). Here we show that AE4-deficient mice exhibit a major dysregulation of acid-base balance. By combining molecular, imaging, biochemical and integrative approaches, we demonstrate that AE4-deficient mice are unable to sense and appropriately correct metabolic alkalosis and acidosis. Mechanistically, a lack of adaptive base secretion via the Cl-/HCO3- exchanger pendrin (Slc26a4) is the key cellular cause of this derailment. Our findings identify AE4 as an essential part of the renal sensing mechanism for changes in acid-base status.

KW - Mice

KW - Animals

KW - Kidney/metabolism

KW - Membrane Transport Proteins/genetics

KW - Acid-Base Equilibrium/physiology

KW - Nephrons/metabolism

KW - Sulfate Transporters/metabolism

KW - Bicarbonates/metabolism

KW - Chloride-Bicarbonate Antiporters

U2 - 10.1038/s41467-023-38562-x

DO - 10.1038/s41467-023-38562-x

M3 - SCORING: Journal article

C2 - 37236964

VL - 14

SP - 3051

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

ER -