Abstract
4-Hydroxynoneal (HNE), an end product of lipid peroxidation, induces apoptosis in many cell types, including neural cells. HNE toxicity is often accompanied by activation of the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) pathway. Here we have evaluated the hypothesis that the primary JNK associated with neurons, JNK3, contributes to HNE-induced neuronal apoptosis. First, we demonstrate that HNE induces caspase-dependent apoptosis in sympathetic neurons. Second, we show that HNE-induced c-Jun phosphorylation and c-jun induction are attenuated in JNK3-deficient neurons. Third, we show that HNE neurotoxicity is significantly inhibited by JNK3 deficiency. In summary, these results indicate that JNK3 plays a critical role in HNE-induced c-Jun activation and apoptosis in sympathetic neurons.
Original language | English |
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Pages (from-to) | 665-670 |
Number of pages | 6 |
Journal | Journal of Neuroscience Research |
Volume | 70 |
Issue number | 5 |
DOIs | |
State | Published - Dec 1 2002 |
Keywords
- Apoptosis
- HNE
- JNK
- Oxidative stress
- Programmed cell death
- Sympathetic neuron
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience