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

Vallet, P.; Charnay, Y.; Steger, K.; Ogier-Denis, E.; Kovari, E.; Herrmann, F.; Michel, J.-P.; Szanto, I.

doi:10.1016/j.neuroscience.2004.12.038

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

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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In situ hybridisation has demonstrated upregulated and persistent cortical NOX4 expression in response to cerebral ischaemia.
“In situ hybridisation has demonstrated upregulated and persistent cortical NOX4 expression in response to cerebral ischaemia [75]”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [75]

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Abstract 149: Endothelial NADPH Oxidase 4 Worsens Ischemic Stroke by Suppressing eNOS Activity
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Abstract 2514: Role of NADPH oxidase 4 in Brain Endothelial Cells after Ischemic Stroke
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Abstract 174: Roles of Pericyte NADPH Oxidase 4 in Acute Brain Ischemia
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NOX4-dependent neuronal autotoxicity and BBB breakdown explain the superior sensitivity of the brain to ischemic damage
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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: Steger, K.
Herrmann, F.
Michel, J.-P.
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: green
archive-ouverte.unige.ch
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuroscience (publishedVersion)
PubMed (publishedVersion)
Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Topics: Health Sciences › Medicine › Physiology › 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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Neuronal expression of the NADPH oxidase NOX4, and its regulation in mouse experimental brain ischemia

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