Korean J Anat.
2009 Dec;42(4):213-218.
Absence Expression of Heat Shock Protein 25 in the Cerebellum of Ataxic Mutant Pogo Mouse
- Affiliations
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- 1Department of Anatomy, College of Medicine, Konyang University, Daejeon, Korea. ygjeong@konyang.ac.kr
- 2Department of Cell Biology & Anatomy, Faculty of Medicine, University of Calgary, Alberta, Canada, T2N 4N1.
- 3Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Abstract
- Heat shock proteins (Hsps) are generally known to be induced in response to a range of stressful stimuli such as hyperthermia, immobilization, UV radiation, arsenite, various chemicals, and drugs. In addition, these proteins have been suggested to have roles in protecting cells against apoptotic cell death. The ataxic mutant Pogo (pogo/pogo) mouse is a novel neurological ataxic mutant, which is derived from Korean wild type mouse (KJR/Mskist) strain. Pogo mutation is considered as an alleles of alpha subunit of P/Q-type calcium channel mutants such as rolling mouse Nagoya (RMN), tottering, and leaner. We investigated the topographical Hsp25 expression using immunohistochemistry and western blot analysis in several ataxic mutant mice: RMN, tottering, leaner, Pogo and Korean wild mouse. In the cerebellum of the RMN, tottering, leaner, and normal mouse including Balb/C, C57BL/6 and ICR mouse, Hsp25 was expressed in a subset of Purkinje cells that form parasagittal stripes. The Hsp25 expression is largely restricted to specific cerebellar lobules: VI /VII (the central zone: CZ), and IX/X (the nodular zone: NZ). Surprisingly, no Hsp25-immunoreactive Purkinje cells were seen in CZ and NZ of the cerebellum of Pogo (pogo/pogo), heterozygotes Pogo (pogo/+), and Korean wild mouse. Moreover, in western blot analysis, there was no cerebellar Hsp25 expression in ataxic Pogo mouse including Korean wild mouse. These data suggest that cerebellar Hsp25 expression was irrelevant with the development of ataxia in Pogo mouse.
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