Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2

Proteinuria promotes chronic kidney disease progression. Karoui et al. show that proteinuria stimulates overexpression of iron transporting protein lipocalin-2 via Ca2+release-induced ER stress, which leads to tubular apoptosis, and that inhibition of this pathway by PBA delays renal deterioration i...

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Main Authors:	Khalil El Karoui, Amandine Viau, Olivier Dellis, Alessia Bagattin, Clément Nguyen, William Baron, Martine Burtin, Mélanie Broueilh, Laurence Heidet, Géraldine Mollet, Anne Druilhe, Corinne Antignac, Bertrand Knebelmann, Gérard Friedlander, Frank Bienaimé, Morgan Gallazzini, Fabiola Terzi
Format:	Article
Language:	English
Published:	Nature Publishing Group 2016-01-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/ncomms10330

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spelling	doaj-84d6beb4c2bc4aa9bafacf3ebe31468b2021-05-11T10:56:49ZengNature Publishing GroupNature Communications2041-17232016-01-017111310.1038/ncomms10330Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2Khalil El Karoui0Amandine Viau1Olivier Dellis2Alessia Bagattin3Clément Nguyen4William Baron5Martine Burtin6Mélanie Broueilh7Laurence Heidet8Géraldine Mollet9Anne Druilhe10Corinne Antignac11Bertrand Knebelmann12Gérard Friedlander13Frank Bienaimé14Morgan Gallazzini15Fabiola Terzi16Département « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesUMR-S 757 INSERM, Université Paris Sud 11, Rue des AdèlesINSERM U1016, CNRS UMR 8104, Université Paris Descartes, Institut CochinDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesINSERM U1163, Université Paris Descartes, Institut Imagine, Hôpital Necker Enfants MaladesINSERM U1163, Université Paris Descartes, Institut Imagine, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesINSERM U1163, Université Paris Descartes, Institut Imagine, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesDépartement « Croissance et Signalisation », Mechanisms and Therapeutic Strategies of Chronic Kidney Disease, INSERM U1151—CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Hôpital Necker Enfants MaladesProteinuria promotes chronic kidney disease progression. Karoui et al. show that proteinuria stimulates overexpression of iron transporting protein lipocalin-2 via Ca2+release-induced ER stress, which leads to tubular apoptosis, and that inhibition of this pathway by PBA delays renal deterioration in proteinuric mice.https://doi.org/10.1038/ncomms10330
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Khalil El Karoui Amandine Viau Olivier Dellis Alessia Bagattin Clément Nguyen William Baron Martine Burtin Mélanie Broueilh Laurence Heidet Géraldine Mollet Anne Druilhe Corinne Antignac Bertrand Knebelmann Gérard Friedlander Frank Bienaimé Morgan Gallazzini Fabiola Terzi
spellingShingle	Khalil El Karoui Amandine Viau Olivier Dellis Alessia Bagattin Clément Nguyen William Baron Martine Burtin Mélanie Broueilh Laurence Heidet Géraldine Mollet Anne Druilhe Corinne Antignac Bertrand Knebelmann Gérard Friedlander Frank Bienaimé Morgan Gallazzini Fabiola Terzi Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2 Nature Communications
author_facet	Khalil El Karoui Amandine Viau Olivier Dellis Alessia Bagattin Clément Nguyen William Baron Martine Burtin Mélanie Broueilh Laurence Heidet Géraldine Mollet Anne Druilhe Corinne Antignac Bertrand Knebelmann Gérard Friedlander Frank Bienaimé Morgan Gallazzini Fabiola Terzi
author_sort	Khalil El Karoui
title	Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2
title_short	Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2
title_full	Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2
title_fullStr	Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2
title_full_unstemmed	Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2
title_sort	endoplasmic reticulum stress drives proteinuria-induced kidney lesions via lipocalin 2
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2016-01-01
description	Proteinuria promotes chronic kidney disease progression. Karoui et al. show that proteinuria stimulates overexpression of iron transporting protein lipocalin-2 via Ca2+release-induced ER stress, which leads to tubular apoptosis, and that inhibition of this pathway by PBA delays renal deterioration in proteinuric mice.
url	https://doi.org/10.1038/ncomms10330
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Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2

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