TY - JOUR
T1 - Extracellular regulated kinase, but not protein kinase C, is an antiapoptotic signal of insulin-like growth factor-1 on cultured cardiac myocytes
AU - Foncea, Rocío
AU - Gálvez, Anita
AU - Pérez, Viviana
AU - Morales, María Paz
AU - Calixto, Andrea
AU - Meléndez, Jaime
AU - González-Jara, Fabián
AU - Díaz-Araya, Guillermo
AU - Sapag-Hagar, Mario
AU - Sugden, Peter H.
AU - Leroith, Derek
AU - Lavandero, Sergio
N1 - 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.
PY - 2000/7/5
Y1 - 2000/7/5
N2 - 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.
AB - 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.
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U2 - 10.1006/bbrc.2000.3008
DO - 10.1006/bbrc.2000.3008
M3 - Article
C2 - 10873673
AN - SCOPUS:0343517544
SN - 0006-291X
VL - 273
SP - 736
EP - 744
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -