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(Stroke. 2006;37:830.)
© 2006 American Heart Association, Inc.

Original Contributions

Upregulated Expression of 14-3-3 Proteins in Astrocytes From Human Cerebrovascular Ischemic Lesions

Yasuhiro Kawamoto, MD; Ichiro Akiguchi, MD; Hidekazu Tomimoto, MD; Yoshitomo Shirakashi, MD; Yasuyuki Honjo, MD Herbert Budka, MD

From the Department of Neurology (Y.K., I.A., H.T., Y.S., Y.H.), Faculty of Medicine, Kyoto University, Japan; and the Institute of Neurology (H.B.), Medical University Vienna, Austria.

Correspondence to Yasuhiro Kawamoto, MD, Department of Neurology, Faculty of Medicine, Kyoto University, 54 Shogoin-Kawaharacho, Sakyoku, Kyoto 606-8507, Japan. E-mail kawamoto{at}kuhp.kyoto-u.ac.jp

Background and Purpose— Several types of chaperone proteins, such as heat shock proteins, have been reported to be associated with brain ischemia. The purpose of this study was to investigate whether an abnormal expression of 14-3-3 proteins, a novel type of molecular chaperones, occurs in human gray and white matter ischemic lesions.

Methods— We prepared formalin-fixed, paraffin-embedded sections from 33 autopsied brains, consisting of 7 normal controls, 4 cases with cerebral thrombosis, 5 cases with cerebral embolism, 8 cases with multiple lacunar infarctions, and 9 cases with Binswanger disease. Deparaffinized sections from all cases were immunostained with anti-14-3-3 antibodies using the avidin-biotin-peroxidase complex method, and some sections were also double-immunostained for 14-3-3 and glial markers.

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.

Key Words: astrocytes • Binswanger disease • cerebral infarction • immunohistochemistry

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