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Neuronal expression of alphaB crystallin in cerebral infarction

alphaB crystallin (alphaBC) is one of the heat shock proteins that are induced under stressful conditions. In normal brains, alphaBC is present in oligodendrocytes and astrocytes, but not in neurons. Neuronal alphaBC expression in the central nervous system under pathological conditions has been inv...

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Bibliographic Details
Published in:Acta neuropathologica 2003-06, Vol.105 (6), p.549-554
Main Authors: Minami, Masayuki, Mizutani, Tomohiko, Kawanishi, Ryuta, Suzuki, Yoshio, Mori, Hiroshi
Format: Article
Language:English
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Summary:alphaB crystallin (alphaBC) is one of the heat shock proteins that are induced under stressful conditions. In normal brains, alphaBC is present in oligodendrocytes and astrocytes, but not in neurons. Neuronal alphaBC expression in the central nervous system under pathological conditions has been investigated in several previous studies, most of which dealt with various neurodegenerative diseases with and without ballooned neurons. Neuronal expression of alphaBC has seldom been studied in cerebral infarction (CI), and the frequency of alphaBC-positive neurons in the various stages of CI is unknown. To investigate this issue, we examined 48 autopsy brains of patients with CI, and found neuronal expression of alphaBC in 68.8% of the cases. We found three types of alphaBC-positive neurons: normal morphological, convex, and ballooned neurons. Although alphaBC-positive neurons were present in the every stage of CI, they were more frequent later than 10 days after the onset of CI, and the frequency of alphaBC-positive ballooned neurons was particularly increased in the later stages of CI. This may indicate that morphologically normal neurons gradually swelled up through convex neurons, finally forming ballooned neurons. Previous studies indicated that alphaBC might have a cytoprotective function as a molecular chaperone, and we speculate that alphaBC is expressed in neurons subjected to ischemic stress, and exerts a cytoprotective effect on the neurons.
ISSN:0001-6322