Renal Na+-K+-Cl- cotransporter activity and vasopressin-induced trafficking are lipid raft-dependent

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Renal Na+-K+-Cl- cotransporter activity and vasopressin-induced trafficking are lipid raft-dependent. / Welker, Pia; Böhlick, Alexandra; Mutig, Kerim; Salanova, Michele; Kahl, Thomas; Schlüter, Hartmut; Blottner, Dieter; Ponce-Coria, Jose; Gamba, Gerardo; Bachmann, Sebastian.

in: AM J PHYSIOL-RENAL, Jahrgang 295, Nr. 3, 3, 09.2008, S. 789-802.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Welker, P, Böhlick, A, Mutig, K, Salanova, M, Kahl, T, Schlüter, H, Blottner, D, Ponce-Coria, J, Gamba, G & Bachmann, S 2008, 'Renal Na+-K+-Cl- cotransporter activity and vasopressin-induced trafficking are lipid raft-dependent', AM J PHYSIOL-RENAL, Jg. 295, Nr. 3, 3, S. 789-802. https://doi.org/10.1152/ajprenal.90227.2008

APA

Welker, P., Böhlick, A., Mutig, K., Salanova, M., Kahl, T., Schlüter, H., Blottner, D., Ponce-Coria, J., Gamba, G., & Bachmann, S. (2008). Renal Na+-K+-Cl- cotransporter activity and vasopressin-induced trafficking are lipid raft-dependent. AM J PHYSIOL-RENAL, 295(3), 789-802. [3]. https://doi.org/10.1152/ajprenal.90227.2008

Vancouver

Bibtex

@article{9149bf0b7b4848c39fbee4f5efd13022,
title = "Renal Na+-K+-Cl- cotransporter activity and vasopressin-induced trafficking are lipid raft-dependent",
abstract = "Apical bumetanide-sensitive Na(+)-K(+)-2Cl(-) cotransporter (NKCC2), the kidney-specific member of a cation-chloride cotransporter superfamily, is an integral membrane protein responsible for the transepithelial reabsorption of NaCl. The role of NKCC2 is essential for renal volume regulation. Vasopressin (AVP) controls NKCC2 surface expression in cells of the thick ascending limb of the loop of Henle (TAL). We found that 40-70% of Triton X-100-insoluble NKCC2 was present in cholesterol-enriched lipid rafts (LR) in rat kidney and cultured TAL cells. The related Na(+)-Cl(-) cotransporter (NCC) from rat kidney was distributed in LR as well. NKCC2-containing LR were detected both intracellularly and in the plasma membrane. Bumetanide-sensitive transport of NKCC2 as analyzed by (86)Rb(+) influx in Xenopus laevis oocytes was markedly reduced by methyl-beta-cyclodextrin (MbetaCD)-induced cholesterol depletion. In TAL, short-term AVP application induced apical vesicular trafficking along with a shift of NKCC2 from non-raft to LR fractions. In parallel, increased colocalization of NKCC2 with the LR ganglioside GM1 and their polar translocation were assessed by confocal analysis. Apical biotinylation showed twofold increases in NKCC2 surface expression. These effects were blunted by mevalonate-lovastatin/MbetaCD-induced cholesterol deprivation. Collectively, these findings demonstrate that a pool of NKCC2 distributes in rafts. Results are consistent with a model in which LR mediate polar insertion, activity, and AVP-induced trafficking of NKCC2 in the control of transepithelial NaCl transport.",
keywords = "Animals, Arginine Vasopressin, Biotinylation, Cell Polarity, Cells, Cultured, Cholesterol, Chromatography, Liquid, Diabetes Insipidus, Neurogenic, Kidney, Loop of Henle, Male, Mass Spectrometry, Membrane Microdomains, Oocytes, Rabbits, Rats, Rats, Long-Evans, Rats, Sprague-Dawley, Receptors, Vasopressin, Sodium-Potassium-Chloride Symporters, Solute Carrier Family 12, Member 1, Xenopus, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "Pia Welker and Alexandra B{\"o}hlick and Kerim Mutig and Michele Salanova and Thomas Kahl and Hartmut Schl{\"u}ter and Dieter Blottner and Jose Ponce-Coria and Gerardo Gamba and Sebastian Bachmann",
year = "2008",
month = sep,
doi = "10.1152/ajprenal.90227.2008",
language = "English",
volume = "295",
pages = "789--802",
journal = "AM J PHYSIOL-RENAL",
issn = "1931-857X",
publisher = "AMER PHYSIOLOGICAL SOC",
number = "3",

}

RIS

TY - JOUR

T1 - Renal Na+-K+-Cl- cotransporter activity and vasopressin-induced trafficking are lipid raft-dependent

AU - Welker, Pia

AU - Böhlick, Alexandra

AU - Mutig, Kerim

AU - Salanova, Michele

AU - Kahl, Thomas

AU - Schlüter, Hartmut

AU - Blottner, Dieter

AU - Ponce-Coria, Jose

AU - Gamba, Gerardo

AU - Bachmann, Sebastian

PY - 2008/9

Y1 - 2008/9

N2 - Apical bumetanide-sensitive Na(+)-K(+)-2Cl(-) cotransporter (NKCC2), the kidney-specific member of a cation-chloride cotransporter superfamily, is an integral membrane protein responsible for the transepithelial reabsorption of NaCl. The role of NKCC2 is essential for renal volume regulation. Vasopressin (AVP) controls NKCC2 surface expression in cells of the thick ascending limb of the loop of Henle (TAL). We found that 40-70% of Triton X-100-insoluble NKCC2 was present in cholesterol-enriched lipid rafts (LR) in rat kidney and cultured TAL cells. The related Na(+)-Cl(-) cotransporter (NCC) from rat kidney was distributed in LR as well. NKCC2-containing LR were detected both intracellularly and in the plasma membrane. Bumetanide-sensitive transport of NKCC2 as analyzed by (86)Rb(+) influx in Xenopus laevis oocytes was markedly reduced by methyl-beta-cyclodextrin (MbetaCD)-induced cholesterol depletion. In TAL, short-term AVP application induced apical vesicular trafficking along with a shift of NKCC2 from non-raft to LR fractions. In parallel, increased colocalization of NKCC2 with the LR ganglioside GM1 and their polar translocation were assessed by confocal analysis. Apical biotinylation showed twofold increases in NKCC2 surface expression. These effects were blunted by mevalonate-lovastatin/MbetaCD-induced cholesterol deprivation. Collectively, these findings demonstrate that a pool of NKCC2 distributes in rafts. Results are consistent with a model in which LR mediate polar insertion, activity, and AVP-induced trafficking of NKCC2 in the control of transepithelial NaCl transport.

AB - Apical bumetanide-sensitive Na(+)-K(+)-2Cl(-) cotransporter (NKCC2), the kidney-specific member of a cation-chloride cotransporter superfamily, is an integral membrane protein responsible for the transepithelial reabsorption of NaCl. The role of NKCC2 is essential for renal volume regulation. Vasopressin (AVP) controls NKCC2 surface expression in cells of the thick ascending limb of the loop of Henle (TAL). We found that 40-70% of Triton X-100-insoluble NKCC2 was present in cholesterol-enriched lipid rafts (LR) in rat kidney and cultured TAL cells. The related Na(+)-Cl(-) cotransporter (NCC) from rat kidney was distributed in LR as well. NKCC2-containing LR were detected both intracellularly and in the plasma membrane. Bumetanide-sensitive transport of NKCC2 as analyzed by (86)Rb(+) influx in Xenopus laevis oocytes was markedly reduced by methyl-beta-cyclodextrin (MbetaCD)-induced cholesterol depletion. In TAL, short-term AVP application induced apical vesicular trafficking along with a shift of NKCC2 from non-raft to LR fractions. In parallel, increased colocalization of NKCC2 with the LR ganglioside GM1 and their polar translocation were assessed by confocal analysis. Apical biotinylation showed twofold increases in NKCC2 surface expression. These effects were blunted by mevalonate-lovastatin/MbetaCD-induced cholesterol deprivation. Collectively, these findings demonstrate that a pool of NKCC2 distributes in rafts. Results are consistent with a model in which LR mediate polar insertion, activity, and AVP-induced trafficking of NKCC2 in the control of transepithelial NaCl transport.

KW - Animals

KW - Arginine Vasopressin

KW - Biotinylation

KW - Cell Polarity

KW - Cells, Cultured

KW - Cholesterol

KW - Chromatography, Liquid

KW - Diabetes Insipidus, Neurogenic

KW - Kidney

KW - Loop of Henle

KW - Male

KW - Mass Spectrometry

KW - Membrane Microdomains

KW - Oocytes

KW - Rabbits

KW - Rats

KW - Rats, Long-Evans

KW - Rats, Sprague-Dawley

KW - Receptors, Vasopressin

KW - Sodium-Potassium-Chloride Symporters

KW - Solute Carrier Family 12, Member 1

KW - Xenopus

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1152/ajprenal.90227.2008

DO - 10.1152/ajprenal.90227.2008

M3 - SCORING: Journal article

C2 - 18579701

VL - 295

SP - 789

EP - 802

JO - AM J PHYSIOL-RENAL

JF - AM J PHYSIOL-RENAL

SN - 1931-857X

IS - 3

M1 - 3

ER -