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  • Title: The transcription factor MEF2C mediates cardiomyocyte hypertrophy induced by IGF-1 signaling.
    Author: Muñoz JP, Collao A, Chiong M, Maldonado C, Adasme T, Carrasco L, Ocaranza P, Bravo R, Gonzalez L, Díaz-Araya G, Hidalgo C, Lavandero S.
    Journal: Biochem Biophys Res Commun; 2009 Oct 09; 388(1):155-60. PubMed ID: 19654000.
    Abstract:
    Myocyte enhancer factor 2C (MEF2C) plays an important role in cardiovascular development and is a key transcription factor for cardiac hypertrophy. Here, we describe MEF2C regulation by insulin-like growth factor-1 (IGF-1) and its role in IGF-1-induced cardiac hypertrophy. We found that IGF-1 addition to cultured rat cardiomyocytes activated MEF2C, as evidenced by its increased nuclear localization and DNA binding activity. IGF-1 stimulated MEF2 dependent-gene transcription in a time-dependent manner, as indicated by increased MEF2 promoter-driven reporter gene activity; IGF-1 also induced p38-MAPK phosphorylation, while an inhibitor of p38-MAPK decreased both effects. Additionally, inhibitors of phosphatidylinositol 3-kinase and calcineurin prevented IGF-1-induced MEF2 transcriptional activity. Via MEF2C-dependent signaling, IGF-1 also stimulated transcription of atrial natriuretic factor and skeletal alpha-actin but not of fos-lux reporter genes. These novel data suggest that MEF2C activation by IGF-1 mediates the pro-hypertrophic effects of IGF-1 on cardiac gene expression.
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