Calcineurin Contributes to the Enhancing Effect of Adenosine on Nerve Growth Factor-Induced Neurite Outgrowth via the Decreased Duration of p38 Mitogen-Activated Protein Kinase Phosphorylation

Adenosine enhances nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells. We found that adenosine increases NGF-induced phosphorylation of extracellular signal-regulated kinase (ERK), but decreases the duration of phosphorylation of p38 mitogen-activated protein (MAP) kinase. Therefore,...

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Bibliographic Details
Published in:Journal of Pharmacological Sciences 2004, Vol.95(1), pp.124-131
Main Authors: Muroi, Yoshikage, Ishii, Toshiaki, Teramoto, Kentarou, Hori, Masatoshi, Nishimura, Masakazu
Format: Article
Language:English
Subjects:
Adenosine - pharmacology
Animals
calcineurin
Calcineurin - pharmacology
Dose-Response Relationship, Drug
Drug Synergism
nerve growth factor
Nerve Growth Factor - pharmacology
neurite outgrowth
Neurites - drug effects
Neurites - enzymology
p38 mitogen-activated protein kinase
p38 Mitogen-Activated Protein Kinases - metabolism
PC12 cell
PC12 Cells
Phosphorylation - drug effects
Rats
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Summary:Adenosine enhances nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells. We found that adenosine increases NGF-induced phosphorylation of extracellular signal-regulated kinase (ERK), but decreases the duration of phosphorylation of p38 mitogen-activated protein (MAP) kinase. Therefore, we further examined the involvement of protein phosphatase in these effects of adenosine. FK506, a specific calcineurin inhibitor, inhibited the enhancing effect of adenosine on the NGF-induced neurite outgrowth and increased the duration of p38 MAP kinase phosphorylation without affecting ERK phosphorylation. These results suggest that adenosine decreases the duration of p38 MAP kinase via calcineurin activation, which contributes to the enhancement of NGF-induced neurite outgrowth.
ISSN:1347-8613
1347-8648
DOI:10.1254/jphs.95.124