파킨슨증후군 유발독소 1-methyl-4-phenylpyridinium에 의한 세포사멸에 있어 카세인키나아제 2 (casein kinase 2)의 역할
Role of Casein Kinase 2 in Parkinsonian Toxin 1-Methyl-4-phenylpyridinium-induced Cell Death
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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.
Abstract
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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