The transcription factor MEF2C mediates cardiomyocyte hypertrophy induced by IGF-1 signaling

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The transcription factor MEF2C mediates cardiomyocyte hypertrophy induced by IGF-1 signaling

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The transcription factor MEF2C mediates cardiomyocyte hypertrophy induced by IGF-1 signaling

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Título: The transcription factor MEF2C mediates cardiomyocyte hypertrophy induced by IGF-1 signaling
Autor: Muñoz, Juan Pablo; Collao, Andrés; Chiong Lay, Mario; Maldonado Vera, Carola Patricia; Adasme, Tatiana; Carrasco Alarcón, Loreto del Pilar; Ocaranza Osses, Paula; Bravo Méndez, Roberto; González, Leticia; Díaz Araya, G.; Hidalgo, Cecilia; Lavandero González, Sergio
Resumen: 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.
URI: http://www.captura.uchile.cl/handle/2250/10998
Fecha: 2009-10-09
Cita del item: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 388 (1): 155-160


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