Cited by 243Nitric Oxide and Endothelin EffectsNeutrophil, Myeloperoxidase and Oxidative MechanismsRedox biology and oxidative stress

NOX2 and NOX4 Mediate Proliferative Response in Endothelial Cells

Petry, Andreas, Djordjevic, Talija, Weitnauer, Michael, Kietzmann, Thomas, Hess, John, Görlach, Agnes·2006·Antioxidants & Redox Signaling

Abstract

Increased levels of reactive oxygen species (ROS) contribute to many cardiovascular diseases. In neutrophils, ROS are generated by a NADPH oxidase containing p22phox and NOX2. NADPH oxidases are also major sources of vascular ROS. Whereas an active NOX2-containing enzyme has been described in endothelial cells, the contribution of recently identified NOX homologues to endothelial ROS production and proliferation has been controversial. The authors, therefore, compared the role of NOX2 with NOX4 and NOX1 in endothelial EaHy926 and human microvascular endothelial cells. NOX2 and NOX4 were abundantly expressed, whereas NOX1 expression was less prominent. NOX2, NOX4, and NOX1 were simultaneously present in a single cell in a perinuclear compartment. NOX2 and NOX4 co-localized with the endoplasmic reticulum (ER) marker calreticulin. Additionally, NOX2 co-localized with F-actin at the plasma membrane. NOX2 and NOX4, which interacted with p22phox, as was shown by bimolecular fluorescent complementation, contributed equally to endothelial ROS production and proliferation, whereas NOX1 depletion did not alter ROS levels under basal conditions. These data show that endothelial cells simultaneously express NOX2, NOX4, and NOX1. NOX2 and NOX4, but not NOX1, equally contributed to ROS generation and proliferation under basal conditions, indicating that a complex relation between NOX homologues controls endothelial function.

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Crossref · 10.1089/ars.2006.8.1473

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Authors
Petry, A., Djordjevic, T., Weitnauer, M., Kietzmann, T., Hess, J., & Görlach, A.
Affiliations
  • Deutsches Herzzentrum München (DE)
  • University of Kaiserslautern (DE)
Venue
Antioxidants & Redox Signaling
Published
2006-09
Volume
8
Issue
9-10
Pages
1473-1484
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
OpenAlex
W1985234565
Cited by
243
References
56
Citations by year
2026: 1 · 2025: 8 · 2024: 3 · 2023: 7 · 2022: 6 · 2021: 9 · 2020: 12 · 2019: 14 · 2018: 8 · 2017: 11 · 2016: 8 · 2015: 12 · 2014: 11 · 2013: 19 · 2012: 21
FWCI
11.93
Type
journal article
Language
en
Open access
closed
Locations
  • Antioxidants and Redox Signaling (publishedVersion)
  • PubMed (publishedVersion)
  • mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
Funders
Deutsche Forschungsgemeinschaft
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
NOX2, NOX4, NOX1, NADPH oxidase, endothelial cells, reactive oxygen species, endothelial cell proliferation, p22phox, calreticulin, endoplasmic reticulum, F-actin, microvascular endothelial cells, EA.hy926 cells, endothelial function
MeSH terms
NADPH Oxidase 1, NADPH Oxidase 2, NADPH Oxidase 4, Actins, Cell Line, Endoplasmic Reticulum, Humans, Membrane Glycoproteins, Microsomes, Phosphorylation, Transfection, Gene Expression, Reactive Oxygen Species, NADPH Oxidases, Protein Interaction Mapping, RNA, Small Interfering, Calreticulin, Endothelial Cells, Protein Kinase Inhibitors, Immunoprecipitation, p38 Mitogen-Activated Protein Kinases, Cell Proliferation

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