Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.

Acyclovir (ACV) is an effective and widely used antiviral agent. However, its clinical application is limited by severe nephrotoxicity. We assessed ACV-induced nephrotoxicity and identified the differentially expressed proteins using mass spectrometry-based proteomic analysis. In total, 30 ICR mice...

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Autores principales:	Hong Lu, Ya-Juan Han, Jia-Dong Xu, Wen-Min Xing, Jie Chen
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c245c241f1e7413f85a6bfc521bbea2e
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spelling	oai:doaj.org-article:c245c241f1e7413f85a6bfc521bbea2e2021-11-25T06:07:22ZProteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.1932-620310.1371/journal.pone.0103185https://doaj.org/article/c245c241f1e7413f85a6bfc521bbea2e2014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25055032/?tool=EBIhttps://doaj.org/toc/1932-6203Acyclovir (ACV) is an effective and widely used antiviral agent. However, its clinical application is limited by severe nephrotoxicity. We assessed ACV-induced nephrotoxicity and identified the differentially expressed proteins using mass spectrometry-based proteomic analysis. In total, 30 ICR mice were intraperitoneally administrated ACV (150 or 600 mg/kg per day) for 9 days. After administration of ACV, levels of serum creatinine and urea nitrogen increased significantly. In addition, mouse kidneys exhibited histopathological changes and reduced expression levels of vascular endothelial growth factor (VEGF) and its receptor VEGFR2. In the proteomic analysis, more than 1,000 proteins were separated by two-dimensional polyacrylamide gel electrophoresis, and a total of 20 proteins were up- or down-regulated in the ACV group compared with the saline group. Among these, six proteins (MHC class II antigen, glyoxalase 1, peroxiredoxin 1, αB-crystallin, fibroblast growth factor receptor 1-IIIb, and cytochrome c oxidase subunit Vb) were identified in association with ACV-induced nephrotoxicity. These findings were confirmed by Western blotting analysis. The differential expression levels of α-BC, Prx1, Glo I and CcO Vb suggest that oxidative damage and mitochondrial injury may be involved in ACV-induced nephrotoxicity. Furthermore, VEGF and FGF may play a role in tissue repair and the restoration process following ACV nephrotoxicity.Hong LuYa-Juan HanJia-Dong XuWen-Min XingJie ChenPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 7, p e103185 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hong Lu Ya-Juan Han Jia-Dong Xu Wen-Min Xing Jie Chen Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.
description	Acyclovir (ACV) is an effective and widely used antiviral agent. However, its clinical application is limited by severe nephrotoxicity. We assessed ACV-induced nephrotoxicity and identified the differentially expressed proteins using mass spectrometry-based proteomic analysis. In total, 30 ICR mice were intraperitoneally administrated ACV (150 or 600 mg/kg per day) for 9 days. After administration of ACV, levels of serum creatinine and urea nitrogen increased significantly. In addition, mouse kidneys exhibited histopathological changes and reduced expression levels of vascular endothelial growth factor (VEGF) and its receptor VEGFR2. In the proteomic analysis, more than 1,000 proteins were separated by two-dimensional polyacrylamide gel electrophoresis, and a total of 20 proteins were up- or down-regulated in the ACV group compared with the saline group. Among these, six proteins (MHC class II antigen, glyoxalase 1, peroxiredoxin 1, αB-crystallin, fibroblast growth factor receptor 1-IIIb, and cytochrome c oxidase subunit Vb) were identified in association with ACV-induced nephrotoxicity. These findings were confirmed by Western blotting analysis. The differential expression levels of α-BC, Prx1, Glo I and CcO Vb suggest that oxidative damage and mitochondrial injury may be involved in ACV-induced nephrotoxicity. Furthermore, VEGF and FGF may play a role in tissue repair and the restoration process following ACV nephrotoxicity.
format	article
author	Hong Lu Ya-Juan Han Jia-Dong Xu Wen-Min Xing Jie Chen
author_facet	Hong Lu Ya-Juan Han Jia-Dong Xu Wen-Min Xing Jie Chen
author_sort	Hong Lu
title	Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.
title_short	Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.
title_full	Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.
title_fullStr	Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.
title_full_unstemmed	Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.
title_sort	proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/c245c241f1e7413f85a6bfc521bbea2e
work_keys_str_mv	AT honglu proteomiccharacterizationofacyclovirinducednephrotoxicityinamousemodel AT yajuanhan proteomiccharacterizationofacyclovirinducednephrotoxicityinamousemodel AT jiadongxu proteomiccharacterizationofacyclovirinducednephrotoxicityinamousemodel AT wenminxing proteomiccharacterizationofacyclovirinducednephrotoxicityinamousemodel AT jiechen proteomiccharacterizationofacyclovirinducednephrotoxicityinamousemodel
_version_	1718414188445958144

Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.

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