Bcl-2 enhances neurite extension via activation of c-Jun N-terminal kinase

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• 作者：Eom ; Dae-Seok ; Choi ; Won-Seok ; Oh ; Young J.
• 关键词：Bcl-2 ; c-Jun N-terminal kinase ; MN9D cells ; Neurite extension ; SNAP-25
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2004
• 出版时间：February 6, 2004
• 年：2004
• 卷：314
• 期：2
• 页码：377-381
• 全文大小：254 K

文摘

Recent studies suggest that Bcl-2 may play an active role in neuronal differentiation. Here, we showed a marked neurite extension in MN9D dopaminergic neuronal cells overexpressing Bcl-2 (MN9D/Bcl-2) or Bcl-X_L (MN9D/Bcl-X_L). We found a specific increase in phosphorylation of c-Jun N-terminal kinase (JNK) accompanied by neurite extension in MN9D/Bcl-2 but not in MN9D/Bcl-X_L cells. Consequently, neurite extension in MN9D/Bcl-2 but not in MN9D/Bcl-X_L cells was suppressed by treatment with SP600125, a specific inhibitor of JNK. Inhibition of other mitogen-activated protein kinases—including p38 and extracellular signal-regulated kinase—did not affect Bcl-2-mediated neurite extension in MN9D cells. While the expression levels of such protein markers of maturation as SNAP-25, phosphorylated NF-H, and neuron-specific enolase were increased in MN9D/Bcl-2 cells, only upregulation of SNAP-25 was inhibited after treatment with SP600125. Thus, the JNK signal activated by Bcl-2 seems to play an important role during morphological and certain biochemical differentiation in cultured dopaminergic neurons.