Involvement of cAMP-dependent protein kinase and pertussis toxin-sensitive G-proteins in CGRP mediated JNK activation in human neuroblastoma cell line

Calcitonin gene-related peptide (CGRP) is a neuropeptide with potent cardiovascular effects, which include positive inotropic and chronotropic actions, systemic vasodilation, and hypotension in animal and human studies. Human neuroblastoma cells (SK-N-MC) have been used as a model system to study th...

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Bibliographic Details
Published in:Neuropeptides (Edinburgh) 2000-06, Vol.34 (3-4), p.229-233
Main Authors: Disa, J., Parameswaran, N., Nambi, P., Aiyar, N.
Format: Article
Language:English
Subjects:
Biological and medical sciences
Calcitonin Gene-Related Peptide - pharmacology
Cell physiology
Cyclic AMP - metabolism
Cyclic AMP-Dependent Protein Kinases - metabolism
Enzyme Activation
Fundamental and applied biological sciences. Psychology
GTP-Binding Proteins - metabolism
Humans
JNK Mitogen-Activated Protein Kinases
Kinetics
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinases - metabolism
Molecular and cellular biology
Neuroblastoma
p38 Mitogen-Activated Protein Kinases
Pertussis Toxin
Phosphorylation
Proto-Oncogene Proteins c-jun - metabolism
Signal transduction
Tumor Cells, Cultured
Virulence Factors, Bordetella - pharmacology
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Summary:Calcitonin gene-related peptide (CGRP) is a neuropeptide with potent cardiovascular effects, which include positive inotropic and chronotropic actions, systemic vasodilation, and hypotension in animal and human studies. Human neuroblastoma cells (SK-N-MC) have been used as a model system to study the CGRP receptors and downstream signaling pathways. This investigation was undertaken to study the role of CGRP in the activation of mitogen-activated protein kinases. While exposure of these cells to CGRP had no significant effect on ERK-1 or p38 MAP kinases, JNK activity was stimulated by CGRP in a time- and concentration-dependent fashion. CGRP-mediated JNK-activation was inhibited by CGRP receptor antagonist, CGRP8–37, confirming that this is a receptor-mediated event. In addition, pretreatment of the cells with H-89, protein kinase A inhibitor or pertussis toxin greatly attenuated CGRP-mediated JNK activation suggesting the requirement of cAMP-dependent protein kinase activation and involvement of pertussis toxin-sensitive G-protein in CGRP-mediated JNK activation.
ISSN:0143-4179
1532-2785
DOI:10.1054/npep.2000.0810