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

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

48 Scopus citations

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 (US)
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
State	Published - Jan 30 1998
Externally published	Yes

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).

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Cardiac hypertrophy
Cardiac myocyte
Heart
Insulin-like growth factor-1
Protein kinase
Signal transduction

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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.",

keywords = "Cardiac hypertrophy, Cardiac myocyte, Heart, Insulin-like growth factor-1, Protein kinase, Signal transduction",

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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doi = "10.1016/S0014-5793(98)00008-8",

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AU - Lavandero, Sergio

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

Y1 - 1998/1/30

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.

KW - Cardiac hypertrophy

KW - Cardiac myocyte

KW - Heart

KW - Insulin-like growth factor-1

KW - Protein kinase

KW - Signal transduction

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ER -

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

Abstract

Bibliographical note

UN SDGs

Keywords

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