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 β-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.
Bibliographical noteFunding Information:
We thank Dr. C.I. Pogson for help with the preparation of the text of this paper. This work was supported in part by Fondo Nacional de Ciencia y Tecnologı́a (FONDECYT) Grants 1950452 (to S.L.) and 2950002 (to R.F.). R.F. is the recipient of a CONICYT fellowship (Chile).
- Cardiac hypertrophy
- Cardiac myocyte
- Insulin-like growth factor-1
- Protein kinase
- Signal transduction