INTRACELLULAR SIGNALING LEADS TO THE HYPERTROPHIC EFFECT OF NEUROPEPTIDE-Y

Citation
Y. Goldberg et al., INTRACELLULAR SIGNALING LEADS TO THE HYPERTROPHIC EFFECT OF NEUROPEPTIDE-Y, American journal of physiology. Cell physiology, 44(5), 1998, pp. 1207-1215
Citations number
37
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Physiology
ISSN journal
0363-6143
Volume
44
Issue
5
Year of publication
1998
Pages
1207 - 1215
Database
ISI
SICI code
0363-6143(1998)44:5<1207:ISLTTH>2.0.ZU;2-7
Abstract
Signal transduction pathways involved in the hypertrophic effect of ne uropeptide Y (NPY) were investigated in adult cardiomyocytes. Reductio n of transforming growth factor-beta activity in serum-supplemented me dia abolished the induction of hypertrophic responsiveness to NPY. In responsive cells, NPY (100 nM) increased protein synthesis, determined as incorporation of [C-14]phenylalanine, by 35 +/- 15% (P < 0.05, n = 16 cultures). In these cells, NPY activated pertussis toxin (PTx)-sen sitive G proteins and phosphatidylinositol (PI) 3-kinase. PTx and inhi bition of PI 3-kinase abolished the hypertrophic effect of NPY. NPY al so activated protein kinase C (PKC) and mitogen-activated protein (MAP ) kinase. Inhibition of these two kinases attenuated the induction of creatine kinase (CK)-BB but not the growth response to NPY. In conclus ion, NPY stimulates protein synthesis in adult cardiomyocytes via acti vation of PTx-sensitive G proteins and PI 3-kinase and it induces the fetal-type CK-BB via activation of PKC and MAP kinase.