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

Dae Seok Eom; Won Seok Choi; Young J. Oh

doi:10.1016/j.bbrc.2003.12.094

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

Dae Seok Eom, Won Seok Choi, Young J. Oh

Department of Systems Biology

Research output: Contribution to journal › Article › peer-review

23 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	377-381
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	314
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2003.12.094
Publication status	Published - 2004 Feb 6

Bibliographical note

Funding 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

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2003.12.094

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title = "Bcl-2 enhances neurite extension via activation of c-Jun N-terminal kinase",

abstract = "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.",

author = "Eom, {Dae Seok} and Choi, {Won Seok} and Oh, {Young J.}",

note = "Funding 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.).",

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N2 - 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.

AB - 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.

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

Abstract

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