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Am J Physiol Cell Physiol 275: C1207-C1215, 1998;
0363-6143/98 $5.00
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Vol. 275, Issue 5, C1207-C1215, November 1998

Intracellular signaling leads to the hypertrophic effect of neuropeptide Y

Yaron Goldberg, Gerhild Taimor, Hans Michael Piper, and Klaus-Dieter Schlüter

Physiologisches Institut, Justus-Liebig-Universität, D-35392 Giessen, Germany

Signal transduction pathways involved in the hypertrophic effect of neuropeptide Y (NPY) were investigated in adult cardiomyocytes. Reduction of transforming growth factor-beta activity in serum-supplemented media abolished the induction of hypertrophic responsiveness to NPY. In responsive cells, NPY (100 nM) increased protein synthesis, determined as incorporation of [14C]phenylalanine, by 35 ± 15% (P < 0.05, n = 16 cultures). In these cells, NPY activated pertussis toxin (PTx)-sensitive G proteins and phosphatidylinositol (PI) 3-kinase. PTx and inhibition of PI 3-kinase abolished the hypertrophic effect of NPY. NPY also 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 conclusion, NPY stimulates protein synthesis in adult cardiomyocytes via activation of PTx-sensitive G proteins and PI 3-kinase and it induces the fetal-type CK-BB via activation of PKC and MAP kinase.

G proteins; phosphatidylinositol 3-kinase; p70s6k; protein kinase C; mitogen-activated protein kinase


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