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PMID: 10865844 Published · ppublish English Journal Article Review

Role of the vascular NADH/NADPH oxidase system in atherosclerosis.

Annals of the New York Academy of Sciences ·Vol. 902 ·2000-05-00 ·Pages 241-7; discussion 247-8

Yokoyama M, Inoue N, Kawashima S

Abstract

It is apparent that vascular tissues can produce reactive oxygen species, including the superoxide anion, and that their increased production can contribute to altered control of vasomotor tone and atherosclerosis. The NADH/NADPH oxidase system, which includes a 22 kD subunit (p22 phox), is the major source of superoxide production in vascular tissues. The superoxide radical oxidizes LDL and oxidized LDL is shown to be a key component in atherogenesis. Superoxide anion inactivates the NO radical, an anti-atherogenic molecule. Lysophosphatidylcholine, which accumulates during oxidative modification of LDL, has multiple effects on vascular cells, including cell proliferation, migration, apoptosis, and gene expression. Lysophosphatidylcholine stimulates superoxide production in endothelial cells through the NADH/NADPH oxidase-dependent mechanism. To investigate the expression of p22 phox in normal and atherosclerotic coronary arteries, samples were obtained from autopsy and examined using immunohistochemistry. In normal vessels, weak positive staining of p22 phox was detectable only in the adventitial layer. In contrast, strong immunoreactivity for p22 phox was present in atherosclerotic lesions around lipid core and shoulder regions. P22 phox was localized in the macrophages, fibroblasts, endothelial cells, and some smooth muscle cells which was identified by immunofluorescence double staining. The genetic analysis of the p22 phox gene by restriction fragment length polymorphism (RFLP) for control subject and patients with coronary artery disease revealed that the prevalence of the TC + TT genotype of the C242T polymorphism of the p22 phox gene in control subjects was significantly more frequent than in coronary artery disease patients, indicating that the mutation of the p22 phox gene might reduce the susceptibility for coronary artery disease, which is independent of other coronary risk factors. These observations suggest that oxidative stress, mainly via the NADH/NADPH oxidase system in the vasculature, may play an important role in the pathogenesis of atherosclerosis.

MeSH Terms
Animals Arteriosclerosis/enzymology,genetics,physiopathology Coronary Disease/genetics,physiopathology Endothelium, Vascular/physiology,physiopathology Humans Membrane Transport Proteins NADH, NADPH Oxidoreductases/genetics,metabolism NADPH Dehydrogenase/genetics NADPH Oxidases Oxidative Stress Phosphoproteins/genetics Polymorphism, Restriction Fragment Length
Chemicals
Membrane Transport Proteins Phosphoproteins NADH, NADPH Oxidoreductases NADPH Oxidases CYBA protein, human NADPH Dehydrogenase
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Yokoyama M
First Department of Internal Medicine, Kobe University School of Medicine, Japan. yokoyama@med.kobe-u.ac.jp
Inoue N
Kawashima S
Article Info
Journal
Annals of the New York Academy of Sciences
Abbr.
Ann N Y Acad Sci
ISSN
0077-8923
Published
2000-05-00
Pages
241-7; discussion 247-8
Language
English
Region
United States
NLM ID
7506858
Subset
IM
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