ArticleJournal of lipid research2009
Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell.
Article in Journal of lipid research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- PPARβ/δ Ligands Regulate Oxidative Status and Inflammatory Response in Inflamed Corpus Luteum-An In Vitro Study.International journal of molecular sciences · 2023Article
- Clinical Significance of Serum Kallistatin and ENOX1 Levels in Patients with Coronary Heart Disease.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2021Article
- Fatty acid epoxyisoprostane E2 stimulates an oxidative stress response in endothelial cells.Biochemical and biophysical research communications · 2014Article
- Role of phospholipid oxidation products in atherosclerosis.Circulation research · 2012Review
- Oxidized phospholipid-induced inflammation is mediated by Toll-like receptor 2.Free radical biology & medicine · 2011Article
- Network for activation of human endothelial cells by oxidized phospholipids: a critical role of heme oxygenase 1.Circulation research · 2011Article
- Circadian blood pressure variability in type 1 diabetes subjects and their nondiabetic siblings - influence of erythrocyte electron transfer.Cardiovascular diabetology · 2010Article
- Systems genetics analysis of gene-by-environment interactions in human cells.American journal of human genetics · 2010Article
- Nrf2 signaling, a mechanism for cellular stress resistance in long-lived mice.Molecular and cellular biology · 2010Article
- NF-E2-related factor 2 regulates the stress response to UVA-1-oxidized phospholipids in skin cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Indolyl-quinuclidinols inhibit ENOX activity and endothelial cell morphogenesis while enhancing radiation-mediated control of tumor vasculature.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- A role for NADPH oxidase 4 in the activation of vascular endothelial cells by oxidized phospholipids.Free radical biology & medicine · 2009Article
- The role of oxidized phospholipids in atherosclerosis.Journal of lipid research · 2009Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Oxidized-1-palmitoyl-2-arachidonyl-sn-glycerol-3-phosphocholine (Ox-PAPC) has been demonstrated to accumulate in atherosclerotic lesions and regulates expression of more than 1,000 genes in human aortic endothelial cell (HAEC). Among the most highly induced is heme oxygenase-1 (HO-1), a cell-protective antioxidant enzyme, which is sensitively induced by oxidative stress. To identify the pathway by which Ox-PAPC induces HO-1, we focused on the plasma membrane electron transport (PMET) complex, which contains ecto-NADH oxidase 1 (eNOX1) and NADPH:quinone oxidoreductase 1 (NQO1) and affects cellular redox status by regulating levels of NAD(P)H. We demonstrated that Ox-PAPC and its active components stimulated electron transfer through the PMET complex in HAECs from inside to outside [as determined by extracellular 2-(4-iodophenyl)-3-(44-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium (WST-1) reduction] and from outside to inside of the cell (as determined by intracellular NBT reduction). Chemical inhibitors of PMET system and siRNAs to PMET components (NQO1 and eNOX1) significantly decreased HO-1 induction by Ox-PAPC. We present evidence that Ox-PAPC activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in HAEC plays an important role in the induction of HO-1 and PMET inhibitors blocked Nrf2 activation by Ox-PAPC. We hypothesized that PMET activation by Ox-PAPC causes intracellular NAD(P)H depletion, which leads to the increased oxidative stress and HO-1 induction. Supporting this hypothesis, cotreatment of cells with exogenous NAD(P)H and Ox-PAPC significantly decreased oxidative stress and HO-1 induction by Ox-PAPC. Taken together, we demonstrated that the PMET system in HAEC plays an important role in the regulation of cellular redox status and HO-1 expression by Ox-PAPC.
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