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Vol. 17, Issue 9, 3978-3988, September 2006
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*Laboratory of Biology of Aging, Department of Rehabilitation and Geriatrics, and ¶Division of Neuropsychiatry, Geneva University Hospitals, 1225 Chêne-Bourg, Switzerland; and #Justus-Liebig-University, Institute of Veterinary Anatomy, Histology, and Embryology, Giessen, Germany
Submitted June 14, 2005;
Revised May 8, 2006;
Accepted June 7, 2006
Monitoring Editor: John Cleveland
Reactive oxygen species (ROS) generated by the NOX family of NADPH oxidases have been described to act as second messengers regulating cell growth and differentiation. However, such a function has hitherto not been convincingly demonstrated. We investigated the role of NOX-derived ROS in cardiac differentiation using mouse embryonic stem cells. ROS scavengers prevented the appearance of spontaneously beating cardiac cells within embryoid bodies. Down-regulation of NOX4, the major NOX isoform present during early stages of differentiation, suppressed cardiogenesis. This was rescued by a pulse of low concentrations of hydrogen peroxide 4 d before spontaneous beating appears. Mechanisms of ROS-dependent signaling included p38 mitogen-activated protein kinase (MAPK) activation and nuclear translocation of the cardiac transcription factor myocyte enhancer factor 2C (MEF2C). Our results provide first molecular evidence that the NOX family of NADPH oxidases regulate vertebrate developmental processes.
These authors contributed equally to this work.
Present addresses: 
Beijing Geriatric Institute, Beijing Hospital, China;
Department of Pathology and Immunology, Faculty of Medicine, Geneva University, 1211 Geneva, Switzerland;
|| Department of Anatomy and Cell Biology and Inflammation Program and Department of Internal Medicine, University of Iowa, Iowa City, IA.
Address correspondence to: Marisa E. Jaconi (marisa.jaconi{at}medecine.unige.ch)
Abbreviations used: CM, cardiomyocytes; EB, embryoid bodies; ESC, embryonic stem cells; EC coupling, excitation-contraction coupling
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