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

FEBS Letters

Foncea, Rocı́o¹  Lavandero, Sergio¹  Pérez, Viviana¹  Sapag-Hagar, Mario¹ 

[1] Departamento de Bioquı́mica y Biologı́a Molecular, Facultad de Ciencias Quı́micas y Farmacéuticas, Universidad de Chile, Casilla 233, Olivos 1007, Santiago, Chile

关键词: Insulin-like growth factor-1;    Heart;    Cardiac myocyte;    Protein kinase;    Signal transduction;    Cardiac hypertrophy;    ERK;    extracellular signal-regulated kinase;    GN;    genistein;    IGF-1;    insulin-like growth factor-1;    IGF-1R;    IGF-1 receptor;    IRS-1;    insulin receptor substrate-1;    MBP;    myelin basic protein;    MEK;    ERK activating kinase;    PD;    PD-098059;    PI3-K;    phosphatidylinositol 3-kinase;    p90 RSK;    p90 S6 kinase;    RP;    rapamycin;    ST;    staurosporine;    TPA;    12-O-tetradecanoylphorbol-13-acetate;    WM;    wortmannin;   

DOI  :  10.1016/S0014-5793(98)00008-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown