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Cited by 291Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative Mechanisms

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

Neuronal expression of the NADPH oxidase NOX4, and its regulation in mouse experimental brain ischemia

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Vallet, P., Charnay, Y., Steger, K., Ogier-Denis, E., Kovari, E., Herrmann, F., Michel, J.-P., Szanto, I.·2005·Neuroscience
DOI 10.1016/j.neuroscience.2004.12.038
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Abstract

Ischemia-induced neuronal damage has been linked to elevated production of reactive oxygen species (ROS) both in animal models and in humans. NADPH oxidase enzymes (NOX-es) are a major enzymatic source of ROS, but their role in brain ischemia has not yet been investigated. The present study was carried out to examine the expression of NOX4, one of the new NADPH oxidase isoforms in a mouse model of focal permanent brain ischemia. We demonstrate that NOX4 is expressed in neurons using in situ hybridization and immunohistochemistry. Ischemia, induced by middle cerebral artery occlusion resulted in a dramatic increase in cortical NOX4 expression. Elevated NOX4 mRNA levels were detectable as early as 24 h after the onset of ischemia and persisted throughout the 30 days of follow-up period, reaching a maximum between days 7 and 15. The early onset suggests neuronal reaction, while the peak period corresponds to the time of neoangiogenesis occurring mainly in the peri-infarct region. The occurrence of NOX4 in the new capillaries was confirmed by immunohistochemical staining. In summary, our paper reports the presence of the ROS producing NADPH oxidase NOX4 in neurons and demonstrates an upregulation of its expression under ischemic conditions. Moreover, a role for NOX4 in ischemia/hypoxia-induced angiogenesis is suggested by its prominent expression in newly formed capillaries.

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Crossref · 10.1016/j.neuroscience.2004.12.038

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Research works printed but not linked: 2

  1. Saran, 2003, To what end does nature produce superoxide?, NADPH oxidase as an autocrine modifier of membrane phospholipids generating paracrine lipid messengers. Free Radic Res, 37, 1045
  2. Soberman, 2003, The expanding network of redox signaling, J Clin Invest, 111, 571, 10.1172/JCI18099 · DOI

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Metadata

Authors
Vallet, P., Charnay, Y., Steger, K., Ogier-Denis, E., Kovari, E., Herrmann, F., Michel, J.-P., & Szanto, I.
Affiliations
University of Geneva (CH)
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
2005-01
Volume
132
Issue
2
Pages
233-238
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/j.neuroscience.2004.12.038
OpenAlex
W1971556924
Cited by
291
References
50
Citations by year
2026: 4 · 2025: 5 · 2024: 7 · 2023: 11 · 2022: 8 · 2021: 10 · 2020: 10 · 2019: 10 · 2018: 13 · 2017: 19 · 2016: 14 · 2015: 11 · 2014: 21 · 2013: 14 · 2012: 26
FWCI
9.79
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords
NOX4, NADPH oxidase, cerebral ischemia, focal cerebral ischemia, middle cerebral artery occlusion, reactive oxygen species, neuronal expression, ischemic neuronal injury, gene upregulation
MeSH terms
NADPH Oxidase 4, Animals, Brain Ischemia, Disease Models, Animal, Immunohistochemistry, Kidney, Functional Laterality, Mice, Inbred C57BL, Neurons, RNA, Messenger, Time Factors, Blotting, Northern, Blotting, Western, Gene Expression Regulation, Enzymologic, In Situ Hybridization, NADPH Oxidases, Reverse Transcriptase Polymerase Chain Reaction, Infarction, Middle Cerebral Artery, Mice

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