NDLI: Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell.

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Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, Sangderk Li, Rongsong Kim, Brandon Palvolgyi, Roland Ho, Tiffany Yang, Qian-Zhou Xu, Jason Szeto, Wan Lam Honda, Henry Berliner, Judith A.
Description	Country affiliation: United States Author Affiliation: Lee S ( Department of Pathology and Laboratory Medicine, University of California-Los Angeles, Los Angeles, CA 90095, USA.)
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.
File Format	HTM / HTML
ISSN	00222275
e-ISSN	15397262
DOI	10.1194/jlr.M800317-JLR200
Journal	The Journal of Lipid Research
Issue Number	2
Volume Number	50
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2009-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Cell Membrane Metabolism Endothelial Cells Heme Oxygenase-1 Genetics Phosphatidylcholines Pharmacology Aorta Cytology Drug Effects Cells, Cultured Electron Transport Gene Expression Models, Biological Nad(p)h Dehydrogenase (quinone) Nadph Oxidase Nf-e2-related Factor 2 Oxidative Stress Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Endocrinology

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Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell*

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Ox-PAPC activation of PMET system increases expression of heme oxygenase-1 in human aortic endothelial cell.