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

doi:10.1006/bbrc.2000.3008

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

Universidad de Chile

Research output: Contribution to journal › Article › peer-review

37 Citations (Scopus)

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 language	English
Pages (from-to)	736-744
Number of pages	9
Journal	Biochemical and Biophysical Research Communications
Volume	273
Issue number	2
DOIs	https://doi.org/10.1006/bbrc.2000.3008
Publication status	Published - 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.

Funding

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.

Funders	Funder number
National Institutes of Health
Comisión Nacional de Investigación Científica y Tecnológica	19980-2063
Fondo Nacional de Ciencia y Tecnología	1980908, 1950452, 296001

ASJC Scopus Subject Areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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Foncea, R., Gálvez, A., Pérez, V., Morales, M. P., Calixto, A., Meléndez, J., González-Jara, F., Díaz-Araya, G., Sapag-Hagar, M., Sugden, P. H., Leroith, D., & Lavandero, S. (2000). Extracellular regulated kinase, but not protein kinase C, is an antiapoptotic signal of insulin-like growth factor-1 on cultured cardiac myocytes. Biochemical and Biophysical Research Communications, 273(2), 736-744. https://doi.org/10.1006/bbrc.2000.3008

Foncea, R, Gálvez, A, Pérez, V, Morales, MP, Calixto, A, Meléndez, J, González-Jara, F, Díaz-Araya, G, Sapag-Hagar, M, Sugden, PH, Leroith, D & Lavandero, S 2000, 'Extracellular regulated kinase, but not protein kinase C, is an antiapoptotic signal of insulin-like growth factor-1 on cultured cardiac myocytes', Biochemical and Biophysical Research Communications, vol. 273, no. 2, pp. 736-744. https://doi.org/10.1006/bbrc.2000.3008

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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.",

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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 Tecnolog{\'i}a (FONDECYT) Grants 1980908 (S.L), 296001 (R.F.), and 1950452 (S.L.) and Cooperaci{\'o}n Internacional NIH– CONICYT Grant 19980-2063 (S.L.). R. Foncea, A. G{\'a}lvez, and F. Gonz{\'a}lez-Jara are recipients of CONICYT fellowships.",

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AU - Morales, María Paz

AU - Calixto, Andrea

AU - Meléndez, Jaime

AU - González-Jara, Fabián

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AU - Sapag-Hagar, Mario

AU - Sugden, Peter H.

AU - Leroith, Derek

AU - Lavandero, Sergio

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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.

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

Abstract

Bibliographical note

Funding

ASJC Scopus Subject Areas

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