ArticleFree radical biology & medicine2012
Nitric oxide reduces NADPH oxidase 5 (Nox5) activity by reversible S-nitrosylation.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 95 citations in OpenAlex.
- F-actin-dependent activation of NADPH oxidase 5 by the vacuolar-type ATPase.The Journal of biological chemistry · 2026Article
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- Regulatory interplay between nitric oxide and heme in redox signaling and inflammation.Redox biology · 2026Review
- Gas entrapping materials for damage control.Advanced drug delivery reviews · 2026Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- PFKFB3 Connects Glycolytic Metabolism with Endothelial Dysfunction in Human and Rodent Obesity.Antioxidants (Basel, Switzerland) · 2025Article
- Mechanism of sodium nitroprusside regulating ginseng quality.Scientific reports · 2025Article
- The role of S-nitrosoglutathione reductase (GSNOR) in T cell-mediated immunopathology of experimental autoimmune encephalomyelitis (EAE).Neuroscience · 2025Article
- The Nitrate-Nitrite-Nitric Oxide Pathway: Potential Role in Mitigating Oxidative Stress in Hypertensive Disorders of Pregnancy.Nutrients · 2024Review
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- NADPH Oxidases: From Molecular Mechanisms to Current Inhibitors.Journal of medicinal chemistry · 2023Review
- A Reappraisal of the Utility of L-012 to Measure Superoxide from Biologically Relevant Sources.Antioxidants (Basel, Switzerland) · 2023Article
- Functional interactions between NADPH oxidase 5 and actin.Frontiers in cell and developmental biology · 2023Article
- Heart-targeted amelioration of sepsis-induced myocardial dysfunction by microenvironment responsive nitric oxide nanogenerators in situ.Journal of nanobiotechnology · 2022Article
- Nitric oxide, chronic iron and copper overloads and regulation of redox homeostasis in rat liver.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2022Article
- NO rapidly mobilizes cellular heme to trigger assembly of its own receptor.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Neuroprotective role of nitric oxide inhalation and nitrite in a Neonatal Rat Model of Hypoxic-Ischemic Injury.PloS one · 2022Article
- Nitric oxide and heme-NO stimulate superoxide production by NADPH oxidase 5.Free radical biology & medicine · 2021Article
- Precision Redox: The Key for Antioxidant Pharmacology.Antioxidants & redox signaling · 2021Review
- Stress-induced reactive oxygen species compartmentalization, perception and signalling.Nature plants · 2021Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The NADPH oxidases (Noxs) are a family of transmembrane oxidoreductases that produce superoxide and other reactive oxygen species (ROS). Nox5 was the last of the conventional Nox isoforms to be identified and is a calcium-dependent enzyme that does not depend on accessory subunits for activation. Recently, Nox5 was shown to be expressed in human blood vessels and therefore the goal of this study was to determine whether nitric oxide (NO) can modulate Nox5 activity. Endogenously produced NO potently inhibited basal and stimulated Nox5 activity and this inhibition was reversible with chronic, but not acute, exposure to L-NAME. Nox5 activity was reduced by NO donors, iNOS, and eNOS and in endothelial cells and LPS-stimulated smooth muscle cells in a manner dependent on NO concentration. ROS production was diminished by NO in an isolated enzyme activity assay replete with surplus calcium and NADPH. There was no evidence for NO-dependent changes in tyrosine nitration, glutathiolation, or phosphorylation of Nox5. In contrast, there was evidence for the increased nitrosylation of Nox5 as determined by the biotin-switch assay and mass spectrometry. Four S-nitrosylation sites were identified and of these, mutation of C694 dramatically lowered Nox5 activity, NO sensitivity, and biotin labeling. Furthermore, coexpression of the denitrosylation enzymes thioredoxin 1 and GSNO reductase prevented NO-dependent inhibition of Nox5. The potency of NO against other Nox enzymes was in the order Nox1 ≥ Nox3 > Nox5 > Nox2, whereas Nox4 was refractory. Collectively, these results suggest that endogenously produced NO can directly S-nitrosylate and inhibit the activity of Nox5.
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