Extracellular regulated kinase, but not protein kinase C, is an antiapoptotic signal of insulin-like growth factor-1 on cultured cardiac myocytes
R Foncea, A Gálvez, V Pérez, MP Morales… - Biochemical and …, 2000 - Elsevier
R Foncea, A Gálvez, V Pérez, MP Morales, A Calixto, J Meléndez, F González-Jara…
Biochemical and biophysical research communications, 2000•ElsevierThis 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 …
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 …
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.
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