Targeting Vascular NADPH Oxidase 1 Blocks Tumor Angiogenesis through a PPARα Mediated Mechanism
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...
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| Published in: | PloS one Vol. 6; no. 2; p. e14665 |
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| Main Authors: | , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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United States
Public Library of Science
07.02.2011
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| ISSN: | 1932-6203, 1932-6203 |
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| Abstract | 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. |
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| AbstractList | 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. 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.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. |
| Author | Heitz, Freddy Page, Patrick Garrido-Urbani, Sarah Deffert, Christine Basset, Olivier Krause, Karl Heinz Rüegg, Curzio Carnesecchi, Stéphanie Michalik, Liliane Szyndralewiez, Cédric Arbiser, Jack Imhof, Beat Jemelin, Stephane Montet, Xavier |
| AuthorAffiliation | 5 Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland 4 Department of Physiology and Metabolism, Centre Médical Universitaire, University of Geneva, Geneva, Switzerland 1 Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Geneva, Switzerland 7 Department of Medicine, Faculty of Science, University of Fribourg, Fribourg, Switzerland 2 Department of Pediatrics, Centre Médical Universitaire, University of Geneva, Geneva, Switzerland 6 Department of Dermatology, Emory University School of Medicine, Atlanta, Georgia, United States of America 3 GenKyoTex S.A., Geneva, Switzerland Universität Heidelberg, Germany |
| AuthorAffiliation_xml | – name: 2 Department of Pediatrics, Centre Médical Universitaire, University of Geneva, Geneva, Switzerland – name: 6 Department of Dermatology, Emory University School of Medicine, Atlanta, Georgia, United States of America – name: Universität Heidelberg, Germany – name: 7 Department of Medicine, Faculty of Science, University of Fribourg, Fribourg, Switzerland – name: 4 Department of Physiology and Metabolism, Centre Médical Universitaire, University of Geneva, Geneva, Switzerland – name: 5 Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland – name: 1 Department of Pathology and Immunology, Centre Médical Universitaire, University of Geneva, Geneva, Switzerland – name: 3 GenKyoTex S.A., Geneva, Switzerland |
| Author_xml | – sequence: 1 givenname: Sarah surname: Garrido-Urbani fullname: Garrido-Urbani, Sarah – sequence: 2 givenname: Stephane surname: Jemelin fullname: Jemelin, Stephane – sequence: 3 givenname: Christine surname: Deffert fullname: Deffert, Christine – sequence: 4 givenname: Stéphanie surname: Carnesecchi fullname: Carnesecchi, Stéphanie – sequence: 5 givenname: Olivier surname: Basset fullname: Basset, Olivier – sequence: 6 givenname: Cédric surname: Szyndralewiez fullname: Szyndralewiez, Cédric – sequence: 7 givenname: Freddy surname: Heitz fullname: Heitz, Freddy – sequence: 8 givenname: Patrick surname: Page fullname: Page, Patrick – sequence: 9 givenname: Xavier surname: Montet fullname: Montet, Xavier – sequence: 10 givenname: Liliane surname: Michalik fullname: Michalik, Liliane – sequence: 11 givenname: Jack surname: Arbiser fullname: Arbiser, Jack – sequence: 12 givenname: Curzio surname: Rüegg fullname: Rüegg, Curzio – sequence: 13 givenname: Karl Heinz surname: Krause fullname: Krause, Karl Heinz – sequence: 14 givenname: Beat surname: Imhof fullname: Imhof, Beat |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21326871$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2011 Garrido-Urbani et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Garrido-Urbani et al. 2011 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Undefined-1 ObjectType-Feature-3 content type line 23 Conceived and designed the experiments: SGU KHK BI. Performed the experiments: SGU SJ CD SC OB CS FH PP. Analyzed the data: SGU. Contributed reagents/materials/analysis tools: CD SC OB CS FH PP XM LM JA CR KHK. Wrote the paper: SGU KHK BI. |
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| Title | Targeting Vascular NADPH Oxidase 1 Blocks Tumor Angiogenesis through a PPARα Mediated Mechanism |
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