ArticleCirculation2016
p22phox C242T Single-Nucleotide Polymorphism Inhibits Inflammatory Oxidative Damage to Endothelial Cells and Vessels.
Article in Circulation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Effect of C242T Polymorphism in the Gene Encoding the NAD(P)H Oxidase p22International journal of environmental research and public health · 2020Trial
- Effect of the CYBA C242T Polymorphism on Preeclampsia Pathogenesis in the Chinese Population.Biochemical genetics · 2024Article
- Molecular Genetics of Abnormal Redox Homeostasis in Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Review
- Regulation of Superoxide by BAP31 through Its Effect on p22Oxidative medicine and cellular longevity · 2021Article
- Nox2 contributes to age-related oxidative damage to neurons and the cerebral vasculature.The Journal of clinical investigation · 2019Article
- NADPH oxidase 2 inhibitors CPP11G and CPP11H attenuate endothelial cell inflammation & vessel dysfunction and restore mouse hind-limb flow.Redox biology · 2019Article
- The matricellular protein TSP1 promotes human and mouse endothelial cell senescence through CD47 and Nox1.Science signaling · 2017Article
- Associations Between Genetic Variants of NADPH Oxidase-Related Genes and Blood Pressure Responses to Dietary Sodium Intervention: The GenSalt Study.American journal of hypertension · 2017Article
- The Pathophysiological Role of NOX2 in Hypertension and Organ Damage.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2016Review
- Computational Models of Reactive Oxygen Species as Metabolic Byproducts and Signal-Transduction Modulators.Frontiers in pharmacology · 2016Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe NADPH oxidase, by generating reactive oxygen species, is involved in the pathophysiology of many cardiovascular diseases and represents a therapeutic target for the development of novel drugs. A single-nucleotide polymorphism, C242T of the p22(phox) subunit of NADPH oxidase, has been reported to be negatively associated with coronary heart disease and may predict disease prevalence. However, the underlying mechanisms remain unknown. METHODS AND
resultsWith the use of computer molecular modeling, we discovered that C242T single-nucleotide polymorphism causes significant structural changes in the extracellular loop of p22(phox) and reduces its interaction stability with Nox2 subunit. Gene transfection of human pulmonary microvascular endothelial cells showed that C242T p22(phox) significantly reduced Nox2 expression but had no significant effect on basal endothelial O2 (.-) production or the expression of Nox1 and Nox4. When cells were stimulated with tumor necrosis factor-α (or high glucose), C242T p22(phox) significantly inhibited tumor necrosis factor-α-induced Nox2 maturation, O2 (.-) production, mitogen-activated protein kinases and nuclear factor κB activation, and inflammation (all P<0.05). These C242T effects were further confirmed using p22(phox) short-hairpin RNA-engineered HeLa cells and Nox2(-/-) coronary microvascular endothelial cells. Clinical significance was investigated by using saphenous vein segments from non-coronary heart disease subjects after phlebotomies. TT (C242T) allele was common (prevalence of ≈22%) and, in comparison with CC, veins bearing TT allele had significantly lower levels of Nox2 expression and O2 (.-) generation in response to high-glucose challenge.
conclusionsC242T single-nucleotide polymorphism causes p22(phox) structural changes that inhibit endothelial Nox2 activation and oxidative response to tumor necrosis factor-α or high-glucose stimulation. C242T single-nucleotide polymorphism may represent a natural protective mechanism against inflammatory cardiovascular diseases.
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