Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease

Studies suggest that Wnt/β-catenin agonists are beneficial in the treatment of acute kidney injury (AKI); however, it remains elusive about its role in the prevention of AKI and its progression to chronic kidney disease (CKD). In this study, renal Wnt/β-catenin signaling was either activated by over...

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Autores principales:	Xue Hong, Yanni Zhou, Dedong Wang, Fuping Lyu, Tianjun Guan, Youhua Liu, Liangxiang Xiao
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	acute kidney injury chronic kidney disease Wnt1 β-catenin ischemia-reperfusion injury Physiology QP1-981
Acceso en línea:	https://doaj.org/article/d82feb5d362e4d9392ad5523ccb87d99
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spelling	oai:doaj.org-article:d82feb5d362e4d9392ad5523ccb87d992021-11-08T07:53:14ZExogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease1664-042X10.3389/fphys.2021.745816https://doaj.org/article/d82feb5d362e4d9392ad5523ccb87d992021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.745816/fullhttps://doaj.org/toc/1664-042XStudies suggest that Wnt/β-catenin agonists are beneficial in the treatment of acute kidney injury (AKI); however, it remains elusive about its role in the prevention of AKI and its progression to chronic kidney disease (CKD). In this study, renal Wnt/β-catenin signaling was either activated by overexpression of exogenous Wnt1 or inhibited by administration with ICG-001, a small molecule inhibitor of β-catenin signaling, before mice were subjected to ischemia/reperfusion injury (IRI) to induce AKI and subsequent CKD. Our results showed that in vivo expression of exogenous Wnt1 before IR protected mice against AKI, and impeded the progression of AKI to CKD in mice, as evidenced by both blood biochemical and kidney histological analyses. In contrast, pre-treatment of ICG-001 before IR had no effect on renal Wnt/β-catenin signaling or the progression of AKI to CKD. Mechanistically, in vivo expression of exogenous Wnt1 before IR suppressed the expression of proapoptotic proteins in AKI mice, and reduced inflammatory responses in both AKI and CKD mice. Additionally, exogenous Wnt1 inhibited apoptosis of tubular cells induced by hypoxia-reoxygenation (H/R) treatment in vitro. To conclude, the present study provides evidences to support the preventive effect of Wnt/β-catenin activation on IR-related AKI and its subsequent progression to CKD.Xue HongYanni ZhouDedong WangFuping LyuTianjun GuanYouhua LiuYouhua LiuLiangxiang XiaoFrontiers Media S.A.articleacute kidney injurychronic kidney diseaseWnt1β-cateninischemia-reperfusion injuryPhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	acute kidney injury chronic kidney disease Wnt1 β-catenin ischemia-reperfusion injury Physiology QP1-981
spellingShingle	acute kidney injury chronic kidney disease Wnt1 β-catenin ischemia-reperfusion injury Physiology QP1-981 Xue Hong Yanni Zhou Dedong Wang Fuping Lyu Tianjun Guan Youhua Liu Youhua Liu Liangxiang Xiao Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease
description	Studies suggest that Wnt/β-catenin agonists are beneficial in the treatment of acute kidney injury (AKI); however, it remains elusive about its role in the prevention of AKI and its progression to chronic kidney disease (CKD). In this study, renal Wnt/β-catenin signaling was either activated by overexpression of exogenous Wnt1 or inhibited by administration with ICG-001, a small molecule inhibitor of β-catenin signaling, before mice were subjected to ischemia/reperfusion injury (IRI) to induce AKI and subsequent CKD. Our results showed that in vivo expression of exogenous Wnt1 before IR protected mice against AKI, and impeded the progression of AKI to CKD in mice, as evidenced by both blood biochemical and kidney histological analyses. In contrast, pre-treatment of ICG-001 before IR had no effect on renal Wnt/β-catenin signaling or the progression of AKI to CKD. Mechanistically, in vivo expression of exogenous Wnt1 before IR suppressed the expression of proapoptotic proteins in AKI mice, and reduced inflammatory responses in both AKI and CKD mice. Additionally, exogenous Wnt1 inhibited apoptosis of tubular cells induced by hypoxia-reoxygenation (H/R) treatment in vitro. To conclude, the present study provides evidences to support the preventive effect of Wnt/β-catenin activation on IR-related AKI and its subsequent progression to CKD.
format	article
author	Xue Hong Yanni Zhou Dedong Wang Fuping Lyu Tianjun Guan Youhua Liu Youhua Liu Liangxiang Xiao
author_facet	Xue Hong Yanni Zhou Dedong Wang Fuping Lyu Tianjun Guan Youhua Liu Youhua Liu Liangxiang Xiao
author_sort	Xue Hong
title	Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease
title_short	Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease
title_full	Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease
title_fullStr	Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease
title_full_unstemmed	Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease
title_sort	exogenous wnt1 prevents acute kidney injury and its subsequent progression to chronic kidney disease
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/d82feb5d362e4d9392ad5523ccb87d99
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Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease

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