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

Sergio Lavandero, Rocío Foncea, Viviana Pérez, Mario Sapag-Hagar

Research output: Contribution to journalArticlepeer-review

44 Scopus citations

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 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.

Original languageEnglish (US)
Pages (from-to)193-196
Number of pages4
JournalFEBS Letters
Volume422
Issue number2
DOIs
StatePublished - Jan 30 1998

Bibliographical note

Funding 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).

Keywords

  • Cardiac hypertrophy
  • Cardiac myocyte
  • Heart
  • Insulin-like growth factor-1
  • Protein kinase
  • Signal transduction

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