Neuropeptide Y (NPY) potentiates phenylephrine-induced mitogen-activated protein kinase activation in primary cardiomyocytes via NPY Y5 receptors
Détails
ID Serval
serval:BIB_59A1B07E968C
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Neuropeptide Y (NPY) potentiates phenylephrine-induced mitogen-activated protein kinase activation in primary cardiomyocytes via NPY Y5 receptors
Périodique
Proceedings of the National Academy of Sciences of the United States of America
ISSN
0027-8424 (Print)
Statut éditorial
Publié
Date de publication
02/2000
Volume
97
Numéro
4
Pages
1595-600
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Feb 15
Research Support, Non-U.S. Gov't --- Old month value: Feb 15
Résumé
Neuropeptide Y (NPY) has been shown to participate in the cardiovascular response mediated by the sympathetic system. In this report, we investigate the growth factor properties of NPY on cardiac myocytes. Mitogen-activated protein kinases (MAPK) are key signaling molecules in the transduction of trophic signals. Therefore, the role of NPY in inducing MAPK activation was studied in mouse neonatal cardiomyocytes. Exposure of neonatal cardiomyocytes to either NPY, phenylephrine, or angiotensin II induces a rapid phosphorylation of the extracellular responsive kinase, the c-jun N-terminal kinase, and the p38 kinase as well as an activation of protein kinase C (PKC). Moreover, NPY potentiates phenylephrine-induced MAPK and PKC stimulation. In contrast, NPY has no synergistic effect on angiotensin II-stimulated MAPK phosphorylation or PKC activity. NPY effects are pertussis toxin-sensitive and calcium-independent and are mediated by NPY Y5 receptors. Taken together, these results suggest that NPY, via G(i) protein-coupled NPY Y5 receptors, could participate in the development of cardiac hypertrophy during chronic sympathetic stimulation by potentiating alpha-adrenergic signals.
Mots-clé
Angiotensin II/pharmacology
Animals
Cells, Cultured
Enzyme Activation/drug effects
Mice
Mice, Inbred C57BL
Mitogen-Activated Protein Kinases/*metabolism
Myocardium/enzymology/*metabolism
Neuropeptide Y/*pharmacology
Pertussis Toxin
Phenylephrine/*pharmacology
Phosphorylation
Protein Kinase C/metabolism
RNA, Messenger/metabolism
Receptors, Neuropeptide Y/*metabolism
Tetradecanoylphorbol Acetate/pharmacology
Thapsigargin/pharmacology
Virulence Factors, Bordetella/pharmacology
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 9:45
Dernière modification de la notice
20/08/2019 15:13