Reoxygenation after severe hypoxia induces cardiomyocyte hypertrophy in vitro: activation of CREB downstream of GSK3ß AMINA EL JAMALI * , CHRISTIAN FREUND, CINDY RECHNER, CLAUS SCHEIDEREIT * , RAINER DIETZ and MARTIN W. BERGMANN 1 Franz-Volhard Clinic, HELIOS Klinikum-Berlin, Charité Campus Buch, Medical Faculty of the Humboldt University Berlin and * Max Delbrück Center for Molecular Medicine, Berlin, Germany 1 Correspondence: Franz Volhard Clinic, Charité Campus Buch, Wiltbergstr. 50, 13125 Berlin, Germany. E-mail: M.Bergmann@mdc-berlin.de <h3>SPECIFIC AIMS</h3> Hypertrophy of viable cardiomyocytes contributes significantly to ventricular remodeling after ischemia/reperfusion in vivo. Our aim was to characterize signaling pathways activated in isolated cardiomyocytes subjected to hypoxia/reoxygenation in relation to protein synthesis focusing on reactive oxygen species (ROS), ß-adrenoreceptors (ß-AR), PI3-kinase, and downstream transcription factors. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Hypoxia/reoxygenation induces cardiomyocyte hypertrophy in vitro</h3> HIF1α protein was stabilized during hypoxia and rapidly degraded during reoxygenation in isolated neonatal rat cardiomyocytes (<h3>Fig. 1</h3> A). 3 H-Leucine incorporation was determined in cells cultured under hypoxia for 1, 3, or 6 h followed by reoxygenation to complete 48 h of culture. Protein synthesis was increased in correlation with prolonged culture under hypoxia. A maximum 1.7 ±0.15-fold increase was observed for 6 h hypoxia, followed by
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Reoxygenation after severe hypoxia induces cardiomyocyte hypertrophy in vitro: activation of CREB downstream of GSK3ß
EL JAMALI, AMINA; FREUND, CHRISTIAN; RECHNER, CINDY; SCHEIDEREIT, CLAUS; DIETZ, RAINER; BERGMANN, MARTIN W.
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, Volume 18 (10): 1096
Fed of American Socs for Experimental Biology – Jul 1, 2004
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