JNK3 contributes to c-jun induction and apoptosis in 4-hydroxynonenal-treated sympathetic neurons

✍ Scribed by Shane R. Bruckner; Steven Estus

• Book ID: 102381359
• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: English
• Weight: 148 KB
• Volume: 70
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.10437

✦ Synopsis

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. © 2002 Wiley‐Liss, Inc.