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Targeting Vascular NADPH Oxidase 1 Blocks Tumor Angiogenesis through a PPARα Mediated Mechanism

  • Garrido-Urbani, Sarah Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Switzerland
  • Jemelin, Stephane Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Switzerland
  • Deffert, Christine Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Switzerland
  • Carnesecchi, Stéphanie Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Switzerland - Department of Pediatrics, Centre Médical Universitaire, University of Geneva, Switzerland
  • Basset, Olivier Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Switzerland
  • Szyndralewiez, Cédric GenKyoTex S.A., Geneva, Switzerland
  • Heitz, Freddy GenKyoTex S.A., Geneva, Switzerland
  • Page, Patrick GenKyoTex S.A., Geneva, Switzerland
  • Montet, Xavier Department of Physiology and Metabolism, Centre Médical Universitaire, University of Geneva, Geneva, Switzerland
  • Michalik, Liliane Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland
  • Arbiser, Jack Department of Dermatology, Emory University School of Medicine, Atlanta, Georgia, United States of America
  • Rüegg, Curzio Department of Medicine, Faculty of Science, University of Fribourg, Switzerland
  • Krause, Karl Heinz Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Switzerland
  • Imhof, Beat A. Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Switzerland
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    07.02.2011
Published in:
  • PLoS ONE. - 2011, vol. 6, no. 2, p. e14665
English Reactive oxygen species, ROS, are regulators of endothelial cell migration, proliferation and survival, events critically involved in angiogenesis. Different isoforms of ROS-generating NOX enzymes are expressed in the vasculature and provide distinct signaling cues through differential localization and activation. We show that mice deficient in NOX1, but not NOX2 or NOX4, have impaired angiogenesis. NOX1 expression and activity is increased in primary mouse and human endothelial cells upon angiogenic stimulation. NOX1 silencing decreases endothelial cell migration and tube-like structure formation, through the inhibition of PPARα, a regulator of NF-κB. Administration of a novel NOX-specific inhibitor reduced angiogenesis and tumor growth in vivo in a PPARα dependent manner. In conclusion, vascular NOX1 is a critical mediator of angiogenesis and an attractive target for anti-angiogenic therapies.
Faculty
Faculté des sciences et de médecine
Department
Médecine 3ème année
Language
  • English
Classification
Biology
License
License undefined
Identifiers
Persistent URL
https://folia.unifr.ch/unifr/documents/301815
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