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KMID : 0359720100280030157
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Journal of the Korean Neurological Association
2010 Volume.28 No. 3 p.157 ~ p.165
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Role of Casein Kinase 2 in Parkinsonian Toxin 1-Methyl-4-phenylpyridinium-induced Cell Death
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Lee Seung-Yeon
Lee Chung-Soo
Han Jung-Ho
Kim Doo-Eung
Hwang Jung-Yun
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Abstract
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Background: Protein casein kinase 2 is involved in signal transduction, cell growth, and apoptosis. However, it has not been elucidated whether parkinsonian toxin 1-methyl-4-phenylpyridinium (MPP + )-induced neuronal cell death is mediated by a casein-kinase-2-mediated pathway.
Methods: We monitored apoptosis-related protein activation, changes in the level of casein kinase 2, nuclear damage, and apoptosis in differentiated PC12 cells exposed to MPP + in combination with casein kinase 2 inhibitor.
Results: Casein kinase 2 inhibitors [4,5,6,7-tetrabromobenzotriazole (TBB), 5,6-dichloro-1-β-D-ribofuranosylbenzimidazole, and apigenin] reduced MPP + - and rotenone-induced cell death in differentiated PC12 cells. TBB inhibited the MPP + -induced activation of apoptosis-related proteins (decreases in Bid and Bcl-2 levels, increase in Bax levels, cytochrome c release, and caspase-3 activation), increase in casein kinase 2 levels, and nuclear damage.
Conclusions: Administering casein kinase 2 inhibitor TBB at concentrations that do not induce toxic effects may reduce MPP + -induced cell death in differentiated PC12 cells by suppressing the apoptosis-related protein activation that leads to cytochrome c release and subsequent activation of caspase-3. The results suggest that MPP + -induced cell death process is mediated by a casein kinase 2 pathway.
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KEYWORD
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4,5,6,7-Tetrabromobenzotriazole, 1-Methyl-4-phenylpyridinium, PC12 cells, Apoptosis-related proteins, Cell death
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