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

doi:10.1016/S0014-5793(98)00008-8

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

Universidad de Chile

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

48 Citations (Scopus)

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 language	English
Pages (from-to)	193-196
Number of pages	4
Journal	FEBS Letters
Volume	422
Issue number	2
DOIs	https://doi.org/10.1016/S0014-5793(98)00008-8
Publication status	Published - 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).

Funding

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).

Funders	Funder number
Comisión Nacional de Investigación Científica y Tecnológica
Fondo Nacional de Ciencia y Tecnología	1950452, 2950002

ASJC Scopus Subject Areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/S0014-5793(98)00008-8

Cite this

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

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.",

author = "Sergio Lavandero and Roc{\'i}o Foncea and Viviana P{\'e}rez and Mario Sapag-Hagar",

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 Tecnolog{\'ı}a (FONDECYT) Grants 1950452 (to S.L.) and 2950002 (to R.F.). R.F. is the recipient of a CONICYT fellowship (Chile).",

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AU - Foncea, Rocío

AU - Pérez, Viviana

AU - Sapag-Hagar, Mario

N1 - 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).

PY - 1998/1/30

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N2 - 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.

AB - 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.

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

Abstract

Bibliographical note

Funding

ASJC Scopus Subject Areas

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