Premium
Differential regulation of JNK in caspase‐3‐mediated apoptosis of MPP + ‐treated primary cortical neurons
Author(s) -
Sun DerShan,
Chang HsinHou
Publication year - 2003
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/s1065-6995(03)00165-3
Subject(s) - apoptosis , mptp , programmed cell death , microbiology and biotechnology , kinase , caspase 3 , caspase , chemistry , protein kinase a , dna fragmentation , biology , neuroscience , biochemistry , dopamine , dopaminergic
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.