Extracellular regulated kinase, but not protein kinase C, is an antiapoptotic signal of insulin-like growth factor-1 on cultured cardiac myocytes

Rocío Foncea, Anita Gálvez, Viviana Pérez, María Paz Morales, Andrea Calixto, Jaime Meléndez, Fabián González-Jara, Guillermo Díaz-Araya, Mario Sapag-Hagar, Peter H. Sugden, Derek Leroith, Sergio Lavandero

Research output: Contribution to journalArticlepeer-review

35 Scopus citations

Abstract

This study aims to elucidate the signaling pathway for insulin-like growth factor-1 (IGF-1) in cultured neonatal rat cardiomyocytes and particularly the role of IGF-1 in cardiac apoptosis. IGF-1 stimulated polyphosphoinositide turnover, translocation of protein kinase C (PKC) isoforms (α, ε, and δ) from the soluble to the particulate fraction, activation of phospholipid-dependent and Ca2+-, phospholipid-dependent PKC, and activation of the extracellular-regulated kinase (ERK). IGF-1 attenuated sorbitol-induced cardiomyocyte viability and nuclear DNA fragmentation. These antiapoptotic effects of IGF-1 were blocked by PD-098059 (an MEK inhibitor) but not by bisindolylmaleimide I (BIM, a specific PKC inhibitor). The ERK pathway may therefore be an important component in the mechanism whereby IGF-1 exerts its antiapoptotic effect on the cardiomyocyte. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)736-744
Number of pages9
JournalBiochemical and Biophysical Research Communications
Volume273
Issue number2
DOIs
StatePublished - Jul 5 2000

Bibliographical note

Funding Information:
We thank Professor C. I. Pogson for help in the preparation of the manuscript. This work was supported in part by Fondo Nacional de Ciencia y Tecnología (FONDECYT) Grants 1980908 (S.L), 296001 (R.F.), and 1950452 (S.L.) and Cooperación Internacional NIH– CONICYT Grant 19980-2063 (S.L.). R. Foncea, A. Gálvez, and F. González-Jara are recipients of CONICYT fellowships.

Keywords

  • Apoptosis
  • Cardiac myocytes
  • Insulin-like growth factor-1
  • Protein kinases
  • Signal transduction

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