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Journal of Biomedicine and Biotechnology
Volume 2009 (2009), Article ID 147946, 8 pages
http://dx.doi.org/10.1155/2009/147946
Research Article

Ischemia Alters the Expression of Connexins in the Aged Human Brain

1Department of Stroke Science, Research Institute for Brain & Blood Vessels-Akita, 6-10 Senshu Kubota Machi, Akita 010-0874, Japan
2Department of Neurology, Research Institute for Brain & Blood Vessels-Akita, 6-10 Senshu Kubota Machi, Akita 010-0874, Japan
3Department of Pathology, Research Institute for Brain & Blood Vessels-Akita, 6-10 Senshu Kubota Machi, Akita 010-0874, Japan

Received 6 April 2009; Revised 8 June 2009; Accepted 30 June 2009

Academic Editor: Thomas van Groen

Copyright © 2009 Taizen Nakase et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Although the function of astrocytic gap junctions under ischemia is still under debate, increased expression of connexin 43 (Cx43) has been observed in ischemic brain lesions, suggesting that astrocytic gap junctions could provide neuronal protection against ischemic insult. Moreover, different connexin subtypes may play different roles in pathological conditions. We used immunohistochemical analysis to investigate alterations in the expression of connexin subtypes in human stroke brains. Seven samples, sectioned after brain embolic stroke, were used for the analysis. Data, evaluated semiquantitatively by computer-assisted densitometry, was compared between the intact hemisphere and ischemic lesions. The results showed that the coexpression of Cx32 and Cx45 with neuronal markers was significantly increased in ischemic lesions. Cx43 expression was significantly increased in the colocalization with astrocytes and relatively increased in the colocalization with neuronal marker in ischemic lesions. Therefore, Cx32, Cx43, and Cx45 may respond differently to ischemic insult in terms of neuroprotection.