Abstract | BACKGROUND AND PURPOSE: METHODS: RESULTS: In the normal control brains, 14-3-3 immunoreactivity was mainly localized to the neuronal somata and processes. Strongly 14-3-3-immunopositive astrocytes were distributed in the infarct lesions and were particularly abundant in infarcts at the chronic stage. Intensely 14-3-3-immunolabeled astrocytes were also observed in the ischemic white matter lesions, and in the severely affected white matter lesions from patients with Binswanger disease, dense 14-3-3 immunoreactivity was found in clasmatodendritic astroglia as well as in reactive astrocytes. CONCLUSIONS: Our results suggest that 14-3-3 proteins may be induced mainly in astrocytes from human cerebrovascular ischemic lesions, and that the upregulated expression of 14-3-3 proteins in astrocytes may be involved in the formation of astrogliosis.
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Authors | Yasuhiro Kawamoto, Ichiro Akiguchi, Hidekazu Tomimoto, Yoshitomo Shirakashi, Yasuyuki Honjo, Herbert Budka |
Journal | Stroke
(Stroke)
Vol. 37
Issue 3
Pg. 830-5
(Mar 2006)
ISSN: 1524-4628 [Electronic] United States |
PMID | 16424378
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- 14-3-3 Proteins
- Glial Fibrillary Acidic Protein
- Protein Isoforms
- Vimentin
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Topics |
- 14-3-3 Proteins
(biosynthesis)
- Aged
- Aged, 80 and over
- Astrocytes
(metabolism)
- Autopsy
- Brain
(anatomy & histology, pathology)
- Brain Infarction
(pathology)
- Cerebral Cortex
(pathology)
- Cerebrovascular Disorders
(metabolism, pathology)
- Dementia, Vascular
(pathology)
- Female
- Frontal Lobe
(pathology)
- Gene Expression Regulation
- Glial Fibrillary Acidic Protein
(metabolism)
- Humans
- Intracranial Embolism
(pathology)
- Intracranial Thrombosis
(pathology)
- Ischemia
(pathology)
- Male
- Middle Aged
- Neuroglia
(pathology)
- Protein Isoforms
- Regression Analysis
- Up-Regulation
- Vimentin
(metabolism)
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