Differential regulation of JNK in caspase-3-mediated apoptosis of MPP(+)-treated primary cortical neurons |
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Authors: | Sun Der-Shan Chang Hsin-Hou |
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Affiliation: | Institute of Human Genetics, Tzu-Chi University, 970 Hualien, Taiwan, ROC. dssun@mail.tcu.edu.tw |
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Abstract: | MPTP (1-methyl-1,2,3,6-tetrahydropyridine), a chemical contaminant of synthetic heroin, induces neuropathological changes with clinical features similar to idiopathic Parkinson's disease. The mechanism by which MPTP and its metabolite MPP(+)(1-methyl-4-phenylpyridinium) induces neuronal cell death remains unclear. We employed primary cortical/telencephalon neuronal cultures to investigate the potential role of caspase and stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK) pathways in MPP(+)-induced neuronal death. DNA fragmentation and caspase-3 activity analysis showed that cortical neuronal cells underwent apoptosis after MPP(+)treatment. However, a basal level of apoptotic cells was also observed in untreated cultures. Interestingly, JNK activity increased in untreated cultures over time, whereas it was down-regulated after MPP(+)treatment. This indicates that the JNK pathways could be differentially regulated in different apoptotic processes. |
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Keywords: | MPP+ Apoptosis Primary cortical neuronal cultures JNK Caspase‐3 |
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