Activation of the ERK cascade by IGF-1 may be responsible for features associated with cardiac myocyte hypertrophy, which can be attenuated by specific signal transduction inhibitors.
Attenuates IGF-1-driven myocyte growth in vitro; leaves open whether ERK inhibition prevents cardiac hypertrophy in vivo.
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.
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Lavandero et al. (1998) studied this question.
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