ArticleFree radical biology & medicine2009
A role for NADPH oxidase 4 in the activation of vascular endothelial cells by oxidized phospholipids.
Article in Free radical biology & medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
- Senescent cells in systemic aging: SASP heterogeneity, immune escape, and endocrine modulation.Biogerontology · 2026Review
- Increased mitochondrial NADPH oxidase 4 (NOX4) expression in aging is a causative factor in aortic stiffening.Redox biology · 2019Article
- Roles of Nicotinamide Adenine Dinucleotide Phosphate (NADPH) Oxidase in Angiogenesis: Isoform-Specific Effects.Antioxidants (Basel, Switzerland) · 2017Review
- NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis.Journal of molecular and cellular cardiology · 2017Article
- Chronic high-magnitude cyclic stretch stimulates EC inflammatory response via VEGF receptor 2-dependent mechanism.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- NADPH oxidase promotes Parkinsonian phenotypes by impairing autophagic flux in an mTORC1-independent fashion in a cellular model of Parkinson's disease.Scientific reports · 2016Article
- Fatty acid epoxyisoprostane E2 stimulates an oxidative stress response in endothelial cells.Biochemical and biophysical research communications · 2014Article
- MicroRNA-146a decreases high glucose/thrombin-induced endothelial inflammation by inhibiting NAPDH oxidase 4 expression.Mediators of inflammation · 2014Article
- Article
- Redox control of inflammation in macrophages.Antioxidants & redox signaling · 2013Review
- New tricks from an old dog: mitochondrial redox signaling in cellular inflammation.Seminars in immunology · 2012Review
- High-density lipoprotein and 4F peptide reduce systemic inflammation by modulating intestinal oxidized lipid metabolism: novel hypotheses and review of literature.Arteriosclerosis, thrombosis, and vascular biology · 2012Review
- Emerging applications for zebrafish as a model organism to study oxidative mechanisms and their roles in inflammation and vascular accumulation of oxidized lipids.Free radical biology & medicine · 2012Review
- Role of phospholipid oxidation products in atherosclerosis.Circulation research · 2012Review
- The NOX toolbox: validating the role of NADPH oxidases in physiology and disease.Cellular and molecular life sciences : CMLS · 2012Review
- Biochemistry, physiology, and pathophysiology of NADPH oxidases in the cardiovascular system.Circulation research · 2012Review
- Metalloproteinase processing of HBEGF is a proximal event in the response of human aortic endothelial cells to oxidized phospholipids.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- Differential regulation of endothelial cell permeability by high and low doses of oxidized 1-palmitoyl-2-arachidonyl-sn-glycero-3-phosphocholine.American journal of respiratory cell and molecular biology · 2012Article
- From form to function: the role of Nox4 in the cardiovascular system.Frontiers in physiology · 2012Article
- A role for VEGFR2 activation in endothelial responses caused by barrier disruptive OxPAPC concentrations.PloS one · 2012Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies from our group have demonstrated that oxidized 1-palmitoyl-2-arachidonyl-sn-glycerol-3-phosphocholine (Ox-PAPC) activates over 1000 genes in human aortic endothelial cells (HAECs). Prominent among these are genes regulating inflammation, cholesterol homeostasis, antioxidant enzymes, and the unfolded protein response. Previous studies from our lab and others suggested that transcriptional regulation by Ox-PAPC may be controlled, at least in part, by reactive oxygen species. We now present evidence that Ox-PAPC activation of NADPH oxidase 4 (NOX4) is responsible for the regulation of two of these important groups of genes: those controlling inflammation and those involved in sterol regulation. Our data demonstrate that Ox-PAPC increases reactive oxygen species formation in HAECs as seen by DCF fluorescence. NOX4 is the major molecule responsible for this increase because downregulation of NOX4 and its components (p22(phox) and rac1) blocked the Ox-PAPC effect. Our data show that Ox-PAPC did not change NOX4 transcription levels but did induce recruitment of rac1 to the membrane for NOX4 activation. We present evidence that vascular endothelial growth factor receptor 2 (VEGFR2) activation is responsible for rac1 recruitment to the membrane. Finally, we demonstrate that knockdown of NOX4 and its components rac1 and p22(phox) decreases Ox-PAPC induction of inflammatory and sterol regulatory genes, but does not affect Ox-PAPC transcriptional regulation of other genes for antioxidants and the unfolded protein response. In summary, we have identified a VEGFR2/NOX4 regulatory pathway by which Ox-PAPC controls important endothelial functions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.