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Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution

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Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution. / Rajaram, Renuga Devi; Dissard, Romain; Faivre, Anna; Ino, Frédérique; Delitsikou, Vasiliki; Jaquet, Vincent; Cagarelli, Thomas; Lindenmeyer, Maja; Jansen-Duerr, Pidder; Cohen, Clemens; Moll, Solange; de Seigneux, Sophie.

in: REDOX BIOL, Jahrgang 2019, Nr. 26, 09.2019, S. 101234.

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

Harvard

Rajaram, RD, Dissard, R, Faivre, A, Ino, F, Delitsikou, V, Jaquet, V, Cagarelli, T, Lindenmeyer, M, Jansen-Duerr, P, Cohen, C, Moll, S & de Seigneux, S 2019, 'Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution', REDOX BIOL, Jg. 2019, Nr. 26, S. 101234. https://doi.org/10.1016/j.redox.2019.101234

APA

Rajaram, R. D., Dissard, R., Faivre, A., Ino, F., Delitsikou, V., Jaquet, V., Cagarelli, T., Lindenmeyer, M., Jansen-Duerr, P., Cohen, C., Moll, S., & de Seigneux, S. (2019). Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution. REDOX BIOL, 2019(26), 101234. https://doi.org/10.1016/j.redox.2019.101234

Vancouver

Rajaram RD, Dissard R, Faivre A, Ino F, Delitsikou V, Jaquet V et al. Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution. REDOX BIOL. 2019 Sep;2019(26):101234. https://doi.org/10.1016/j.redox.2019.101234

Bibtex

@article{496a9bbb3f0b485bb1b858ff5c45b9a8,
title = "Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution",
abstract = "BACKGROUND: NADPH oxidase 4 (NOX4) catalyzes the formation of hydrogen peroxide (H2O2). NOX4 is highly expressed in the kidney, but its role in renal injury is unclear and may depend on its specific tissue localization.METHODS: We performed immunostaining with a specific anti-NOX4 antibody and measured NOX4 mRNA expression in human renal biopsies encompassing diverse renal diseases. We generated transgenic mice specifically overexpressing mouse Nox4 in renal tubular cells and subjected the animals to the unilateral ureteral obstruction (UUO) model of fibrosis.RESULTS: In normal human kidney, NOX4 protein expression was at its highest on the basolateral side of proximal tubular cells. NOX4 expression increased in mesangial cells and podocytes in proliferative diabetic nephropathy. In tubular cells, NOX4 protein expression decreased in all types of chronic renal disease studied. This finding was substantiated by decreased NOX4 mRNA expression in the tubulo-interstitial compartment in a repository of 175 human renal biopsies. Overexpression of tubular NOX4 in mice resulted in enhanced renal production of H2O2, increased NRF2 protein expression and decreased glomerular filtration, likely via stimulation of the tubulo-glomerular feedback. Tubular NOX4 overexpression had no obvious impact on kidney morphology, apoptosis, or fibrosis at baseline. Under acute and chronic tubular injury induced by UUO, overexpression of NOX4 in tubular cells did not modify the course of the disease.CONCLUSIONS: NOX4 expression was decreased in tubular cells in all types of CKD tested. Tubular NOX4 overexpression did not induce injury in the kidney, and neither modified microvascularization, nor kidney structural lesions in fibrosis.",
author = "Rajaram, {Renuga Devi} and Romain Dissard and Anna Faivre and Fr{\'e}d{\'e}rique Ino and Vasiliki Delitsikou and Vincent Jaquet and Thomas Cagarelli and Maja Lindenmeyer and Pidder Jansen-Duerr and Clemens Cohen and Solange Moll and {de Seigneux}, Sophie",
note = "Copyright {\textcopyright} 2019 The Authors. Published by Elsevier B.V. All rights reserved.",
year = "2019",
month = sep,
doi = "10.1016/j.redox.2019.101234",
language = "English",
volume = "2019",
pages = "101234",
journal = "REDOX BIOL",
issn = "2213-2317",
publisher = "Elsevier BV",
number = "26",

}

RIS

TY - JOUR

T1 - Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution

AU - Rajaram, Renuga Devi

AU - Dissard, Romain

AU - Faivre, Anna

AU - Ino, Frédérique

AU - Delitsikou, Vasiliki

AU - Jaquet, Vincent

AU - Cagarelli, Thomas

AU - Lindenmeyer, Maja

AU - Jansen-Duerr, Pidder

AU - Cohen, Clemens

AU - Moll, Solange

AU - de Seigneux, Sophie

N1 - Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.

PY - 2019/9

Y1 - 2019/9

N2 - BACKGROUND: NADPH oxidase 4 (NOX4) catalyzes the formation of hydrogen peroxide (H2O2). NOX4 is highly expressed in the kidney, but its role in renal injury is unclear and may depend on its specific tissue localization.METHODS: We performed immunostaining with a specific anti-NOX4 antibody and measured NOX4 mRNA expression in human renal biopsies encompassing diverse renal diseases. We generated transgenic mice specifically overexpressing mouse Nox4 in renal tubular cells and subjected the animals to the unilateral ureteral obstruction (UUO) model of fibrosis.RESULTS: In normal human kidney, NOX4 protein expression was at its highest on the basolateral side of proximal tubular cells. NOX4 expression increased in mesangial cells and podocytes in proliferative diabetic nephropathy. In tubular cells, NOX4 protein expression decreased in all types of chronic renal disease studied. This finding was substantiated by decreased NOX4 mRNA expression in the tubulo-interstitial compartment in a repository of 175 human renal biopsies. Overexpression of tubular NOX4 in mice resulted in enhanced renal production of H2O2, increased NRF2 protein expression and decreased glomerular filtration, likely via stimulation of the tubulo-glomerular feedback. Tubular NOX4 overexpression had no obvious impact on kidney morphology, apoptosis, or fibrosis at baseline. Under acute and chronic tubular injury induced by UUO, overexpression of NOX4 in tubular cells did not modify the course of the disease.CONCLUSIONS: NOX4 expression was decreased in tubular cells in all types of CKD tested. Tubular NOX4 overexpression did not induce injury in the kidney, and neither modified microvascularization, nor kidney structural lesions in fibrosis.

AB - BACKGROUND: NADPH oxidase 4 (NOX4) catalyzes the formation of hydrogen peroxide (H2O2). NOX4 is highly expressed in the kidney, but its role in renal injury is unclear and may depend on its specific tissue localization.METHODS: We performed immunostaining with a specific anti-NOX4 antibody and measured NOX4 mRNA expression in human renal biopsies encompassing diverse renal diseases. We generated transgenic mice specifically overexpressing mouse Nox4 in renal tubular cells and subjected the animals to the unilateral ureteral obstruction (UUO) model of fibrosis.RESULTS: In normal human kidney, NOX4 protein expression was at its highest on the basolateral side of proximal tubular cells. NOX4 expression increased in mesangial cells and podocytes in proliferative diabetic nephropathy. In tubular cells, NOX4 protein expression decreased in all types of chronic renal disease studied. This finding was substantiated by decreased NOX4 mRNA expression in the tubulo-interstitial compartment in a repository of 175 human renal biopsies. Overexpression of tubular NOX4 in mice resulted in enhanced renal production of H2O2, increased NRF2 protein expression and decreased glomerular filtration, likely via stimulation of the tubulo-glomerular feedback. Tubular NOX4 overexpression had no obvious impact on kidney morphology, apoptosis, or fibrosis at baseline. Under acute and chronic tubular injury induced by UUO, overexpression of NOX4 in tubular cells did not modify the course of the disease.CONCLUSIONS: NOX4 expression was decreased in tubular cells in all types of CKD tested. Tubular NOX4 overexpression did not induce injury in the kidney, and neither modified microvascularization, nor kidney structural lesions in fibrosis.

U2 - 10.1016/j.redox.2019.101234

DO - 10.1016/j.redox.2019.101234

M3 - SCORING: Journal article

C2 - 31247506

VL - 2019

SP - 101234

JO - REDOX BIOL

JF - REDOX BIOL

SN - 2213-2317

IS - 26

ER -