Abstract
The endoplasmic reticulum (ER) is thought to play important roles in various neurological diseases via multifactorial and complex mechanisms. The Ire1-mediated signal is part of one ER signaling pathways; the signal induces the expression of an ER-resident protein, Bip/GRP78, and is thought to be involved in cell death under ER stress. In this study, we examined time-dependent Bip expression after transient middle cerebral artery occlusion and characterized the Bip-positive cells. Ire1- mediated molecules, Bip, were rapidly up-regulated in the ischemic area after 3.5 h recirculation. Their immunoreactivity continued to increase until 24-48 h. Immunofluorescence staining revealed Bip up-regulation in ischemic neurons, which were TUNEL positive. Our studies suggest that the Ire1-mediated signal might be associated with ischemic neuronal damage.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Carrier Proteins / analysis
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Carrier Proteins / genetics*
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DNA Fragmentation
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Endoplasmic Reticulum / chemistry
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Endoplasmic Reticulum Chaperone BiP
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Fluorescent Antibody Technique
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Gene Expression / physiology
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Heat-Shock Proteins*
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Infarction, Middle Cerebral Artery / pathology
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Infarction, Middle Cerebral Artery / physiopathology
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Ischemic Attack, Transient / pathology
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Ischemic Attack, Transient / physiopathology*
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Male
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Membrane Proteins*
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Molecular Chaperones / analysis
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Molecular Chaperones / genetics*
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Neurons / chemistry
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Neurons / pathology
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Protein Serine-Threonine Kinases / physiology*
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RNA, Messenger / analysis
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Rats
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Rats, Sprague-Dawley
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Signal Transduction / physiology
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Stroke / pathology
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Stroke / physiopathology
Substances
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Carrier Proteins
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Endoplasmic Reticulum Chaperone BiP
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Heat-Shock Proteins
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Membrane Proteins
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Molecular Chaperones
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RNA, Messenger
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Ern2 protein, rat
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Protein Serine-Threonine Kinases