DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation

Summary: The “preconditioning effect” in AKI is a phenomenon in which an episode of ischemia-reperfusion results in tolerance to subsequent ischemia-reperfusion injury. However, its relationship between DNA damage repair has not been elucidated. Here, we show the role of KAT5 in the preconditioning...

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Autores principales:	Akihito Hishikawa, Kaori Hayashi, Akiko Kubo, Kazutoshi Miyashita, Akinori Hashiguchi, Kenichiro Kinouchi, Norifumi Yoshimoto, Ran Nakamichi, Riki Akashio, Erina Sugita, Tatsuhiko Azegami, Toshiaki Monkawa, Makoto Suematsu, Hiroshi Itoh
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Pathophysiology Cell biology Science Q
Acceso en línea:	https://doaj.org/article/b9104add2d57440785cf3e54283a323b
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spelling	oai:doaj.org-article:b9104add2d57440785cf3e54283a323b2021-11-28T04:36:22ZDNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation2589-004210.1016/j.isci.2021.103436https://doaj.org/article/b9104add2d57440785cf3e54283a323b2021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2589004221014073https://doaj.org/toc/2589-0042Summary: The “preconditioning effect” in AKI is a phenomenon in which an episode of ischemia-reperfusion results in tolerance to subsequent ischemia-reperfusion injury. However, its relationship between DNA damage repair has not been elucidated. Here, we show the role of KAT5 in the preconditioning effect. Preconditioning attenuated DNA damage in proximal tubular cells with elevated KAT5 expression. Ischemia-reperfusion (IR) injuries were exacerbated, and preconditioning effect vanished in proximal tubular-cell-specific KAT5 knockout mice. Investigation of tubuloglomerular feedback (TGF) by MALDI-IMS and urinary adenosine revealed that preconditioning caused attenuated TGF at least in part via KAT5. In addition, K-Cl cotransporter 3 (KCC3) expression decreased in damaged proximal tubular cells, which may be involved in accelerated TGF following IR. Furthermore, KAT5 induced KCC3 expression by maintaining chromatin accessibility and binding to the KCC3 promoter. These results suggest a novel mechanism of the preconditioning effect mediated by the promotion of DNA repair and attenuation of TGF through KAT5.Akihito HishikawaKaori HayashiAkiko KuboKazutoshi MiyashitaAkinori HashiguchiKenichiro KinouchiNorifumi YoshimotoRan NakamichiRiki AkashioErina SugitaTatsuhiko AzegamiToshiaki MonkawaMakoto SuematsuHiroshi ItohElsevierarticlePathophysiologyCell biologyScienceQENiScience, Vol 24, Iss 12, Pp 103436- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Pathophysiology Cell biology Science Q
spellingShingle	Pathophysiology Cell biology Science Q Akihito Hishikawa Kaori Hayashi Akiko Kubo Kazutoshi Miyashita Akinori Hashiguchi Kenichiro Kinouchi Norifumi Yoshimoto Ran Nakamichi Riki Akashio Erina Sugita Tatsuhiko Azegami Toshiaki Monkawa Makoto Suematsu Hiroshi Itoh DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation
description	Summary: The “preconditioning effect” in AKI is a phenomenon in which an episode of ischemia-reperfusion results in tolerance to subsequent ischemia-reperfusion injury. However, its relationship between DNA damage repair has not been elucidated. Here, we show the role of KAT5 in the preconditioning effect. Preconditioning attenuated DNA damage in proximal tubular cells with elevated KAT5 expression. Ischemia-reperfusion (IR) injuries were exacerbated, and preconditioning effect vanished in proximal tubular-cell-specific KAT5 knockout mice. Investigation of tubuloglomerular feedback (TGF) by MALDI-IMS and urinary adenosine revealed that preconditioning caused attenuated TGF at least in part via KAT5. In addition, K-Cl cotransporter 3 (KCC3) expression decreased in damaged proximal tubular cells, which may be involved in accelerated TGF following IR. Furthermore, KAT5 induced KCC3 expression by maintaining chromatin accessibility and binding to the KCC3 promoter. These results suggest a novel mechanism of the preconditioning effect mediated by the promotion of DNA repair and attenuation of TGF through KAT5.
format	article
author	Akihito Hishikawa Kaori Hayashi Akiko Kubo Kazutoshi Miyashita Akinori Hashiguchi Kenichiro Kinouchi Norifumi Yoshimoto Ran Nakamichi Riki Akashio Erina Sugita Tatsuhiko Azegami Toshiaki Monkawa Makoto Suematsu Hiroshi Itoh
author_facet	Akihito Hishikawa Kaori Hayashi Akiko Kubo Kazutoshi Miyashita Akinori Hashiguchi Kenichiro Kinouchi Norifumi Yoshimoto Ran Nakamichi Riki Akashio Erina Sugita Tatsuhiko Azegami Toshiaki Monkawa Makoto Suematsu Hiroshi Itoh
author_sort	Akihito Hishikawa
title	DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation
title_short	DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation
title_full	DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation
title_fullStr	DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation
title_full_unstemmed	DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation
title_sort	dna repair factor kat5 prevents ischemic acute kidney injury through glomerular filtration regulation
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/b9104add2d57440785cf3e54283a323b
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DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation

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