Analysis of Spatial and Temporal Protein Expression in the Cerebral Cortex after Ischemia-Reperfusion Injury.
- Author:
Yuan Hao CHEN
1
;
Yung Hsiao CHIANG
;
Hsin I MA
Author Information
- Publication Type:Original Article
- Keywords: reperfusion injury; proteomics; protein expression; cerebral ischemia; neurodegenerative mechanisms; gerontology
- MeSH: Aconitate Hydratase; Aged; Anoxia; Brain Injuries; Brain Ischemia; Carotid Arteries; Cerebral Cortex*; Dynamin I; Fructose-Bisphosphate Aldolase; Geriatrics; Heat-Shock Proteins; Humans; Ischemia; Ligation; Male; Mass Spectrometry; Proteome; Proteomics; Rats, Sprague-Dawley; Reperfusion Injury*
- From:Journal of Clinical Neurology 2014;10(2):84-93
- CountryRepublic of Korea
- Language:English
- 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.
