ArticleThe Biochemical journal2006
Homocysteine stimulates phosphorylation of NADPH oxidase p47phox and p67phox subunits in monocytes via protein kinase Cbeta activation.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 92 citations in OpenAlex.
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- Hyperhomocysteinemia: Underlying Links to Stroke and Hydrocephalus, with a Focus on Polyphenol-Based Therapeutic Approaches.Nutrients · 2024Review
- One-Carbon and Polyamine Metabolism as Cancer Therapy Targets.Biomolecules · 2022Review
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- Association of Promoter Methylation and Expression of Inflammatory Genes IL-6 and TNF-α with the Risk of Coronary Artery Disease in Diabetic and Obese Subjects among Asian Indians.Indian journal of clinical biochemistry : IJCB · 2022Article
- Folic acid, either solely or combined with L-citrulline, improves NO signaling and ameliorates chronic hypoxia-induced pulmonary hypertension in newborn pigs.Physiological reports · 2021Article
- Effects of Vitamin BAntioxidants (Basel, Switzerland) · 2021Article
- High-dose folic acid supplementation results in significant accumulation of unmetabolized homocysteine, leading to severe oxidative stress in Caenorhabditis elegans.Redox biology · 2020Article
- Distinct Redox Signalling following Macrophage Activation Influences Profibrotic Activity.Journal of immunology research · 2019Article
- Pioglitazone restores the homocysteine‑impaired function of endothelial progenitor cells via the inhibition of the protein kinase C/NADPH oxidase pathway.Molecular medicine reports · 2018Article
- Redox regulation of the actin cytoskeleton and its role in the vascular system.Free radical biology & medicine · 2017Review
- Vitamin BRedox biology · 2017Article
- PKC/NADPH oxidase are involved in the protective effect of pioglitazone in high homocysteine-induced paracrine dyfunction in endothelial progenitor cells.American journal of translational research · 2017Article
- Vascular endothelial dysfunction and pharmacological treatment.World journal of cardiology · 2015Review
- Association of Aberrations in One Carbon Metabolism with Intimal Medial Thickening in Patients with Type 2 Diabetes Mellitus.Indian journal of clinical biochemistry : IJCB · 2015Article
- Docetaxel Facilitates Endothelial Dysfunction through Oxidative Stress via Modulation of Protein Kinase C Beta: The Protective Effects of Sotrastaurin.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Lipid-induced NOX2 activation inhibits autophagic flux by impairing lysosomal enzyme activity.Journal of lipid research · 2015Article
- Purinergic signaling mediates oxidative stress in UVA-exposed THP-1 cells.Toxicology reports · 2015Article
- GCPII modulates oxidative stress and prostate cancer susceptibility through changes in methylation of RASSF1, BNIP3, GSTP1 and Ec-SOD.Molecular biology reports · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Hyperhomocysteinaemia is an independent risk factor for cardiovascular diseases due to atherosclerosis. The development of atherosclerosis involves reactive oxygen species-induced oxidative stress in vascular cells. Our previous study [Wang and O (2001) Biochem. J. 357, 233-240] demonstrated that Hcy (homocysteine) treatment caused a significant elevation of intracellular superoxide anion, leading to increased expression of chemokine receptor in monocytes. NADPH oxidase is primarily responsible for superoxide anion production in monocytes. In the present study, we investigated the molecular mechanism of Hcy-induced superoxide anion production in monocytes. Hcy treatment (20-100 microM) caused an activation of NADPH oxidase and an increase in the superoxide anion level in monocytes (THP-1, a human monocytic cell line). Transfection of cells with p47phox siRNA (small interfering RNA) abolished Hcy-induced superoxide anion production, indicating the involvement of NADPH oxidase. Hcy treatment resulted in phosphorylation and subsequently membrane translocation of p47phox and p67phox subunits leading to NADPH oxidase activation. Pretreatment of cells with PKC (protein kinase C) inhibitors Ro-32-0432 (bisindolylmaleimide XI hydrochloride) (selective for PKCalpha, PKCbeta and PKCgamma) abolished Hcy-induced phosphorylation of p47phox and p67phox subunits in monocytes. Transfection of cells with antisense PKCbeta oligonucleotide, but not antisense PKCalpha oligonucleotide, completely blocked Hcy-induced phosphorylation of p47phox and p67phox subunits as well as superoxide anion production. Pretreatment of cells with LY333531, a PKCbeta inhibitor, abolished Hcy-induced superoxide anion production. Taken together, these results indicate that Hcy-stimulated superoxide anion production in monocytes is regulated through PKC-dependent phosphorylation of p47phox and p67phox subunits of NADPH oxidase. Increased superoxide anion production via NADPH oxidase may play an important role in Hcy-induced inflammatory response during atherogenesis.
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