Analysis of spatial and temporal protein expression in the cerebral cortex after Ischemia-Reperfusion injury

Yuan Hao Chen, Yung-Hsiao Chiang, Hsin I. Maa

研究成果: 雜誌貢獻文章

8 引文 (Scopus)

摘要

Background and Purpose Hypoxia, or ischemia, is a common cause of neurological deficits in the elderly. This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae. Methods Cerebral ischemia was induced in male Sprague-Dawley rats by transient ligation of the left carotid artery followed by 60 min of hypoxia. A two-dimensional differential proteome analysis was performed using matrix-assisted laser desorption ionization-time-of-flight mass spectrometry to compare changes in protein expression on the lesioned side of the cortex relative to that on the contralateral side at 0, 6, and 24 h after ischemia. Results The expressions of the following five proteins were up-regulated in the ipsilateral cortex at 24 h after ischemia-reperfusion injury compared to the contralateral (i.e., control) side: aconitase 2, neurotensin-related peptide, hypothetical protein XP-212759, 60-kDa heatshock protein, and aldolase A. The expression of one protein, dynamin-1, was up-regulated only at the 6-h time point. The level of 78-kDa glucose-regulated protein precursor on the lesioned side of the cerebral cortex was found to be high initially, but then down-regulated by 24 h after the induction of ischemia-reperfusion injury. The expressions of several metabolic enzymes and translational factors were also perturbed soon after brain ischemia. Conclusions These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.
原文英語
頁(從 - 到)84-93
頁數10
期刊Journal of Clinical Neurology (Korea)
10
發行號2
DOIs
出版狀態已發佈 - 2014

指紋

Spatio-Temporal Analysis
Reperfusion Injury
Cerebral Cortex
Brain Ischemia
Ischemia
Proteins
Dynamin I
Aconitate Hydratase
Neurotensin
Fructose-Bisphosphate Aldolase
Protein Precursors
Staphylococcal Protein A
Proteome
Carotid Arteries
Brain Injuries
Ligation
Sprague Dawley Rats
Mass Spectrometry
Lasers
Glucose

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

引用此文

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title = "Analysis of spatial and temporal protein expression in the cerebral cortex after Ischemia-Reperfusion injury",
abstract = "Background and Purpose Hypoxia, or ischemia, is a common cause of neurological deficits in the elderly. This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae. Methods Cerebral ischemia was induced in male Sprague-Dawley rats by transient ligation of the left carotid artery followed by 60 min of hypoxia. A two-dimensional differential proteome analysis was performed using matrix-assisted laser desorption ionization-time-of-flight mass spectrometry to compare changes in protein expression on the lesioned side of the cortex relative to that on the contralateral side at 0, 6, and 24 h after ischemia. Results The expressions of the following five proteins were up-regulated in the ipsilateral cortex at 24 h after ischemia-reperfusion injury compared to the contralateral (i.e., control) side: aconitase 2, neurotensin-related peptide, hypothetical protein XP-212759, 60-kDa heatshock protein, and aldolase A. The expression of one protein, dynamin-1, was up-regulated only at the 6-h time point. The level of 78-kDa glucose-regulated protein precursor on the lesioned side of the cerebral cortex was found to be high initially, but then down-regulated by 24 h after the induction of ischemia-reperfusion injury. The expressions of several metabolic enzymes and translational factors were also perturbed soon after brain ischemia. Conclusions These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.",
keywords = "Cerebral ischemia, Gerontology, Neurodegenerative mechanisms, Protein expression, Proteomics, Reperfusion injury",
author = "Chen, {Yuan Hao} and Yung-Hsiao Chiang and Maa, {Hsin I.}",
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T1 - Analysis of spatial and temporal protein expression in the cerebral cortex after Ischemia-Reperfusion injury

AU - Chen, Yuan Hao

AU - Chiang, Yung-Hsiao

AU - Maa, Hsin I.

PY - 2014

Y1 - 2014

N2 - Background and Purpose Hypoxia, or ischemia, is a common cause of neurological deficits in the elderly. This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae. Methods Cerebral ischemia was induced in male Sprague-Dawley rats by transient ligation of the left carotid artery followed by 60 min of hypoxia. A two-dimensional differential proteome analysis was performed using matrix-assisted laser desorption ionization-time-of-flight mass spectrometry to compare changes in protein expression on the lesioned side of the cortex relative to that on the contralateral side at 0, 6, and 24 h after ischemia. Results The expressions of the following five proteins were up-regulated in the ipsilateral cortex at 24 h after ischemia-reperfusion injury compared to the contralateral (i.e., control) side: aconitase 2, neurotensin-related peptide, hypothetical protein XP-212759, 60-kDa heatshock protein, and aldolase A. The expression of one protein, dynamin-1, was up-regulated only at the 6-h time point. The level of 78-kDa glucose-regulated protein precursor on the lesioned side of the cerebral cortex was found to be high initially, but then down-regulated by 24 h after the induction of ischemia-reperfusion injury. The expressions of several metabolic enzymes and translational factors were also perturbed soon after brain ischemia. Conclusions These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.

AB - Background and Purpose Hypoxia, or ischemia, is a common cause of neurological deficits in the elderly. This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae. Methods Cerebral ischemia was induced in male Sprague-Dawley rats by transient ligation of the left carotid artery followed by 60 min of hypoxia. A two-dimensional differential proteome analysis was performed using matrix-assisted laser desorption ionization-time-of-flight mass spectrometry to compare changes in protein expression on the lesioned side of the cortex relative to that on the contralateral side at 0, 6, and 24 h after ischemia. Results The expressions of the following five proteins were up-regulated in the ipsilateral cortex at 24 h after ischemia-reperfusion injury compared to the contralateral (i.e., control) side: aconitase 2, neurotensin-related peptide, hypothetical protein XP-212759, 60-kDa heatshock protein, and aldolase A. The expression of one protein, dynamin-1, was up-regulated only at the 6-h time point. The level of 78-kDa glucose-regulated protein precursor on the lesioned side of the cerebral cortex was found to be high initially, but then down-regulated by 24 h after the induction of ischemia-reperfusion injury. The expressions of several metabolic enzymes and translational factors were also perturbed soon after brain ischemia. Conclusions These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.

KW - Cerebral ischemia

KW - Gerontology

KW - Neurodegenerative mechanisms

KW - Protein expression

KW - Proteomics

KW - Reperfusion injury

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