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

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

Research output: Contribution to journalArticle

9 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)84-93
Number of pages10
JournalJournal of Clinical Neurology (Korea)
Volume10
Issue number2
DOIs
Publication statusPublished - 2014

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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

Keywords

  • Cerebral ischemia
  • Gerontology
  • Neurodegenerative mechanisms
  • Protein expression
  • Proteomics
  • Reperfusion injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

Cite this

Analysis of spatial and temporal protein expression in the cerebral cortex after Ischemia-Reperfusion injury. / Chen, Yuan Hao; Chiang, Yung-Hsiao; Maa, Hsin I.

In: Journal of Clinical Neurology (Korea), Vol. 10, No. 2, 2014, p. 84-93.

Research output: Contribution to journalArticle

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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.

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KW - Proteomics

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