Abstract
IGF-1 increased 2-fold protein synthesis in cardiac myocytes. Genistein, whether added during preincubation or with IGF-1 at the start of incubation, significantly inhibited the IGF-1-induced stimulation of protein synthesis, autophosphorylation of the beta-subunit of IGF-1 receptor and inhibition of ERK. When added 1 or 6 h after IGF-1, however, genistein was without effect. IGF-1-stimulated protein synthesis was also significantly inhibited by PD-098059, staurosporine, and rapamycin, but not by wortmannin, in cardiac myocytes. Some inhibitors produced a reduction in cell size. Activation of the ERK cascade by IGF-1 may be responsible for some of the features associated with cardiac myocyte hypertrophy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Androstadienes / pharmacology
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Animals
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Animals, Newborn
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Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Cardiomegaly
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Cells, Cultured
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Enzyme Inhibitors / pharmacology*
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Flavonoids / pharmacology
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Genistein / pharmacology
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Heart / drug effects*
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Heart Ventricles
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Insulin-Like Growth Factor I / pharmacology*
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Myocardium / cytology
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Myocardium / metabolism*
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Phosphorylation
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Polyenes / pharmacology
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Protein Biosynthesis*
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Rats
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Rats, Sprague-Dawley
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Receptor, IGF Type 1 / metabolism*
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Signal Transduction / drug effects
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Signal Transduction / physiology*
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Sirolimus
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Staurosporine / pharmacology
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Wortmannin
Substances
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Androstadienes
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Enzyme Inhibitors
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Flavonoids
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Polyenes
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Insulin-Like Growth Factor I
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Genistein
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Receptor, IGF Type 1
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Calcium-Calmodulin-Dependent Protein Kinases
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Staurosporine
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2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one
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Sirolimus
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Wortmannin