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-XL). 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-XL cells. Consequently, neurite extension in MN9D/Bcl-2 but not in MN9D/Bcl-XL 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.
|Number of pages||5|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - 2004 Feb 6|
Bibliographical noteFunding Information:
We thank Dr. George J. Markelonis for his critical reading of our manuscript. This work was supported by a grant from the KRF (E00109 and DP0519), and in part by the Ministry of Health and Welfare (HMP-00-CH-13-0012), the KOSEF through the Brain Disease Research Center at Ajou University, and the MOST (M1-0108-00-0096 and NM-2-44 to Y.J.O.).
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology