Analysis of Spatial and Temporal Protein Expression in the Cerebral Cortex after Ischemia-Reperfusion Injury
Journal of Clinical Neurology 2014³â 10±Ç 2È£ p.84 ~ p.93
(Chen Yuan-Hao) - National Defense Medical Center Tri-Service General Hospital Department of Neurological Surgery
(Chiang Yung-Hsiao) - Taipei Medical University Taipei Medical University Hospital Department of Surgery
(Ma Hsin-I) - National Defense Medical Center Tri-Service General Hospital Department of Neurological Surgery
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 heat-shock 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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reperfusion injury, proteomics, protein expression, cerebral ischemia, neurodegenerative mechanisms, gerontology
KMID :
1130620140100020084
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