Effect of inhibitors of signal transduction on IGF-1-induced protein synthesis associated with hypertrophy in cultured neonatal rat ventricular myocytes

Lavandero S.; Foncea, R; Pérez V; Sapag-Hagar, M

Keywords: muscle, growth, flavonoids, rat, size, enzyme, biosynthesis, heart, animals, phosphorylation, synthesis, culture, rats, protein, cell, hypertrophy, genistein, transduction, receptor, newborn, vitro, signal, wortmannin, inhibitors, article, kinase, myocardium, factor, staurosporine, sirolimus, type, controlled, ventricle, animal, autophosphorylation, rapamycin, c, study, 1, 3, amino, priority, in, nonhuman, journal, Animalia, Rats,, Sprague-Dawley, 2, (2, Cells,, Cultured, Receptor,, I, Animals,, dependent, activated, Cardiomegaly, Ventricles, somatomedin, Insulin-Like, mitogen, Ca(2+)-Calmodulin, methoxyphenyl)chromone, Androstadienes, Polyenes, IGF


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 ?-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.

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Título de la Revista: FEBS LETTERS
Volumen: 422
Número: 2
Editorial: Elsevier
Fecha de publicación: 1998
Página de inicio: 193
Página final: 196
URL: http://www.scopus.com/inward/record.url?eid=2-s2.0-0032579211&partnerID=q2rCbXpz