In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury

Oxidative stress plays an important role in the pathophysiology of acute kidney injury (AKI). Previously, we reported that vanin-1, which is involved in oxidative stress, is associated with renal tubular injury. This study was aimed to determine whether urinary vanin-1 is a biomarker for the early d...

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Autores principales:	Keiko Hosohata, Denan Jin, Shinji Takai
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	sensitive biomarker renal tubular damage ischemia-reperfusion Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/f01a1e22e0eb425c805cd88d3cfed590
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spelling	oai:doaj.org-article:f01a1e22e0eb425c805cd88d3cfed5902021-11-11T16:54:41ZIn Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury10.3390/ijms2221114481422-00671661-6596https://doaj.org/article/f01a1e22e0eb425c805cd88d3cfed5902021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11448https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Oxidative stress plays an important role in the pathophysiology of acute kidney injury (AKI). Previously, we reported that vanin-1, which is involved in oxidative stress, is associated with renal tubular injury. This study was aimed to determine whether urinary vanin-1 is a biomarker for the early diagnosis of AKI in two experimental models: in vivo and in vitro. In a rat model of AKI, ischemic AKI was induced in uninephrectomized rats by clamping the left renal artery for 45 min and then reperfusing the kidney. On Day 1 after renal ischemia/reperfusion (I/R), serum creatinine (SCr) in I/R rats was higher than in sham-operated rats, but this did not reach significance. Urinary N-acetyl-β-D-glucosaminidase (NAG) exhibited a significant increase but decreased on Day 2 in I/R rats. In contrast, urinary vanin-1 significantly increased on Day 1 and remained at a significant high level on Day 2 in I/R rats. Renal vanin-1 protein decreased on Days 1 and 3. In line with these findings, immunofluorescence staining demonstrated that vanin-1 was attenuated in the renal proximal tubules of I/R rats. Our in vitro results confirmed that the supernatant from HK-2 cells under hypoxia/reoxygenation included significantly higher levels of vanin-1 as well as KIM-1 and NGAL. In conclusion, our results suggest that urinary vanin-1 might be a potential novel biomarker of AKI induced by I/R.Keiko HosohataDenan JinShinji TakaiMDPI AGarticlesensitive biomarkerrenal tubular damageischemia-reperfusionBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11448, p 11448 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	sensitive biomarker renal tubular damage ischemia-reperfusion Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	sensitive biomarker renal tubular damage ischemia-reperfusion Biology (General) QH301-705.5 Chemistry QD1-999 Keiko Hosohata Denan Jin Shinji Takai In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury
description	Oxidative stress plays an important role in the pathophysiology of acute kidney injury (AKI). Previously, we reported that vanin-1, which is involved in oxidative stress, is associated with renal tubular injury. This study was aimed to determine whether urinary vanin-1 is a biomarker for the early diagnosis of AKI in two experimental models: in vivo and in vitro. In a rat model of AKI, ischemic AKI was induced in uninephrectomized rats by clamping the left renal artery for 45 min and then reperfusing the kidney. On Day 1 after renal ischemia/reperfusion (I/R), serum creatinine (SCr) in I/R rats was higher than in sham-operated rats, but this did not reach significance. Urinary N-acetyl-β-D-glucosaminidase (NAG) exhibited a significant increase but decreased on Day 2 in I/R rats. In contrast, urinary vanin-1 significantly increased on Day 1 and remained at a significant high level on Day 2 in I/R rats. Renal vanin-1 protein decreased on Days 1 and 3. In line with these findings, immunofluorescence staining demonstrated that vanin-1 was attenuated in the renal proximal tubules of I/R rats. Our in vitro results confirmed that the supernatant from HK-2 cells under hypoxia/reoxygenation included significantly higher levels of vanin-1 as well as KIM-1 and NGAL. In conclusion, our results suggest that urinary vanin-1 might be a potential novel biomarker of AKI induced by I/R.
format	article
author	Keiko Hosohata Denan Jin Shinji Takai
author_facet	Keiko Hosohata Denan Jin Shinji Takai
author_sort	Keiko Hosohata
title	In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury
title_short	In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury
title_full	In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury
title_fullStr	In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury
title_full_unstemmed	In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury
title_sort	in vivo and in vitro evaluation of urinary biomarkers in ischemia/reperfusion-induced kidney injury
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/f01a1e22e0eb425c805cd88d3cfed590
work_keys_str_mv	AT keikohosohata invivoandinvitroevaluationofurinarybiomarkersinischemiareperfusioninducedkidneyinjury AT denanjin invivoandinvitroevaluationofurinarybiomarkersinischemiareperfusioninducedkidneyinjury AT shinjitakai invivoandinvitroevaluationofurinarybiomarkersinischemiareperfusioninducedkidneyinjury
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In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury

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