Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury

Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI). Many investigators have reported that cell death via apoptosis significantly contributed to the pathophysiology of renal IRI. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tu...

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Main Authors:	Adachi, Takaomi, Sugiyama, Noriyuki, Gondai, Tatsuro, Yagita, Hideo, Yokoyama, Takahiko
Format:	Online
Language:	English
Published:	Japan Society of Histochemistry and Cytochemistry 2013
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929614/

id	pubmed-3929614
recordtype	oai_dc
spelling	pubmed-39296142014-04-01 Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury Adachi, Takaomi Sugiyama, Noriyuki Gondai, Tatsuro Yagita, Hideo Yokoyama, Takahiko Regular Article Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI). Many investigators have reported that cell death via apoptosis significantly contributed to the pathophysiology of renal IRI. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor superfamily, and induces apoptosis and inflammation. However, the role of TRAIL in renal IRI is unclear. Here, we investigated whether TRAIL contributes to renal IRI and whether TRAIL blockade could attenuate renal IRI. AKI was induced by unilateral clamping of the renal pedicle for 60 min in male FVB/N mice. We found that the expression of TRAIL and its receptors were highly upregulated in renal tubular cells in renal IRI. Neutralizing anti-TRAIL antibody or its control IgG was given 24 hr before ischemia and a half-dose booster injection was administered into the peritoneal cavity immediately after reperfusion. We found that TRAIL blockade inhibited tubular apoptosis and reduced the accumulation of neutrophils and macrophages. Furthermore, TRAIL blockade attenuated renal fibrosis and atrophy after IRI. In conclusion, our study suggests that TRAIL is a critical pathogenic factor in renal IRI, and that TRAIL could be a new therapeutic target for the prevention of renal IRI. Japan Society of Histochemistry and Cytochemistry 2013-12-28 2013-11-22 /pmc/articles/PMC3929614/ /pubmed/24610963 http://dx.doi.org/10.1267/ahc.13022 Text en © 2013 The Japan Society of Histochemistry and Cytochemistry This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Adachi, Takaomi Sugiyama, Noriyuki Gondai, Tatsuro Yagita, Hideo Yokoyama, Takahiko
spellingShingle	Adachi, Takaomi Sugiyama, Noriyuki Gondai, Tatsuro Yagita, Hideo Yokoyama, Takahiko Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury
author_facet	Adachi, Takaomi Sugiyama, Noriyuki Gondai, Tatsuro Yagita, Hideo Yokoyama, Takahiko
author_sort	Adachi, Takaomi
title	Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury
title_short	Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury
title_full	Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury
title_fullStr	Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury
title_full_unstemmed	Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury
title_sort	blockade of death ligand trail inhibits renal ischemia reperfusion injury
description	Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI). Many investigators have reported that cell death via apoptosis significantly contributed to the pathophysiology of renal IRI. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor superfamily, and induces apoptosis and inflammation. However, the role of TRAIL in renal IRI is unclear. Here, we investigated whether TRAIL contributes to renal IRI and whether TRAIL blockade could attenuate renal IRI. AKI was induced by unilateral clamping of the renal pedicle for 60 min in male FVB/N mice. We found that the expression of TRAIL and its receptors were highly upregulated in renal tubular cells in renal IRI. Neutralizing anti-TRAIL antibody or its control IgG was given 24 hr before ischemia and a half-dose booster injection was administered into the peritoneal cavity immediately after reperfusion. We found that TRAIL blockade inhibited tubular apoptosis and reduced the accumulation of neutrophils and macrophages. Furthermore, TRAIL blockade attenuated renal fibrosis and atrophy after IRI. In conclusion, our study suggests that TRAIL is a critical pathogenic factor in renal IRI, and that TRAIL could be a new therapeutic target for the prevention of renal IRI.
publisher	Japan Society of Histochemistry and Cytochemistry
publishDate	2013
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929614/
_version_	1612060145480630272

Blockade of Death Ligand TRAIL Inhibits Renal Ischemia Reperfusion Injury

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