GlutaredoxinV1, Main, Exploration, bibRecord, 000786

Ambient ultrafine particles reduce endothelial nitric oxide production via S-glutathionylation of eNOS.

Identifieur interne : 000786 ( Main/Exploration ); précédent : 000785; suivant : 000787

Ambient ultrafine particles reduce endothelial nitric oxide production via S-glutathionylation of eNOS.

Auteurs : Yunfeng Du [États-Unis] ; Mohamad Navab ; Melody Shen ; James Hill ; Payam Pakbin ; Constantinos Sioutas ; Tzung K. Hsiai ; Rongsong Li

Source :

Biochemical and biophysical research communications [ 1090-2104 ] ; 2013.

RBID : pubmed:23751346

Descripteurs français

KwdFr :
- Activation enzymatique (MeSH), Acétophénones (pharmacologie), Animaux (MeSH), Anthracènes (pharmacologie), Aorte (cytologie), Biomimétique (MeSH), Cellules cultivées (MeSH), Cellules endothéliales (effets des médicaments et des substances chimiques), Cellules endothéliales (métabolisme), Endothélium vasculaire (cytologie), Glutathion (métabolisme), Humains (MeSH), Marqueurs de spin (MeSH), Matière particulaire (métabolisme), Monoxyde d'azote (biosynthèse), Métalloporphyrines (pharmacologie), N-oxydes cycliques (pharmacologie), NADPH oxidase (antagonistes et inhibiteurs), Nitric oxide synthase type III (métabolisme), Oxydoréduction (MeSH), Souris (MeSH), Stress oxydatif (MeSH), Superoxide dismutase (antagonistes et inhibiteurs), Superoxide dismutase-1 (MeSH), Taille de particule (MeSH).
MESH :
- antagonistes et inhibiteurs : NADPH oxidase, Superoxide dismutase.
- biosynthèse : Monoxyde d'azote.
- cytologie : Aorte, Endothélium vasculaire.
- effets des médicaments et des substances chimiques : Cellules endothéliales.
- métabolisme : Cellules endothéliales, Glutathion, Matière particulaire, Nitric oxide synthase type III.
- pharmacologie : Acétophénones, Anthracènes, Métalloporphyrines, N-oxydes cycliques.
- Activation enzymatique, Animaux, Biomimétique, Cellules cultivées, Humains, Marqueurs de spin, Oxydoréduction, Souris, Stress oxydatif, Superoxide dismutase-1, Taille de particule.

English descriptors

KwdEn :
- Acetophenones (pharmacology), Animals (MeSH), Anthracenes (pharmacology), Aorta (cytology), Biomimetics (MeSH), Cells, Cultured (MeSH), Cyclic N-Oxides (pharmacology), Endothelial Cells (drug effects), Endothelial Cells (metabolism), Endothelium, Vascular (cytology), Enzyme Activation (MeSH), Glutathione (metabolism), Humans (MeSH), Metalloporphyrins (pharmacology), Mice (MeSH), NADPH Oxidases (antagonists & inhibitors), Nitric Oxide (biosynthesis), Nitric Oxide Synthase Type III (metabolism), Oxidation-Reduction (MeSH), Oxidative Stress (MeSH), Particle Size (MeSH), Particulate Matter (metabolism), Spin Labels (MeSH), Superoxide Dismutase (antagonists & inhibitors), Superoxide Dismutase-1 (MeSH).
MESH :
- chemical , antagonists & inhibitors : NADPH Oxidases, Superoxide Dismutase.
- chemical , biosynthesis : Nitric Oxide.
- chemical , metabolism : Glutathione, Nitric Oxide Synthase Type III, Particulate Matter.
- chemical , pharmacology : Acetophenones, Anthracenes, Cyclic N-Oxides, Metalloporphyrins.
- cytology : Aorta, Endothelium, Vascular.
- drug effects : Endothelial Cells.
- metabolism : Endothelial Cells.
- Animals, Biomimetics, Cells, Cultured, Enzyme Activation, Humans, Mice, Oxidation-Reduction, Oxidative Stress, Particle Size, Spin Labels, Superoxide Dismutase-1.

Abstract

Exposure to airborne particulate pollutants is intimately linked to vascular oxidative stress and inflammatory responses with clinical relevance to atherosclerosis. Particulate matter (PM) has been reported to induce endothelial dysfunction and atherosclerosis. Here, we tested whether ambient ultrafine particles (UFP, diameter <200 nm) modulate eNOS activity in terms of nitric oxide (NO) production via protein S-glutathionylation. Treatment of human aortic endothelial cells (HAEC) with UFP significantly reduced NO production. UFP-mediated reduction in NO production was restored in the presence of JNK inhibitor (SP600125), NADPH oxidase inhibitor (Apocynin), anti-oxidant (N-acetyl cysteine), and superoxide dismutase mimetics (Tempol and MnTMPyP). UFP exposure increased the GSSG/GSH ratio and eNOS S-glutathionylation, whereas over-expression of Glutaredoxin-1 (to inhibit S-glutathionylation) restored UFP-mediated reduction in NO production by nearly 80%. Thus, our findings suggest that eNOS S-glutathionylation is a potential mechanism underlying ambient UFP-induced reduction of NO production.

DOI: 10.1016/j.bbrc.2013.05.127
PubMed: 23751346
PubMed Central: PMC3743434

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000734
to stream Main, to step Curation: 000734

Le document en format XML

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<front><div type="abstract" xml:lang="en">Exposure to airborne particulate pollutants is intimately linked to vascular oxidative stress and inflammatory responses with clinical relevance to atherosclerosis. Particulate matter (PM) has been reported to induce endothelial dysfunction and atherosclerosis. Here, we tested whether ambient ultrafine particles (UFP, diameter <200 nm) modulate eNOS activity in terms of nitric oxide (NO) production via protein S-glutathionylation. Treatment of human aortic endothelial cells (HAEC) with UFP significantly reduced NO production. UFP-mediated reduction in NO production was restored in the presence of JNK inhibitor (SP600125), NADPH oxidase inhibitor (Apocynin), anti-oxidant (N-acetyl cysteine), and superoxide dismutase mimetics (Tempol and MnTMPyP). UFP exposure increased the GSSG/GSH ratio and eNOS S-glutathionylation, whereas over-expression of Glutaredoxin-1 (to inhibit S-glutathionylation) restored UFP-mediated reduction in NO production by nearly 80%. Thus, our findings suggest that eNOS S-glutathionylation is a potential mechanism underlying ambient UFP-induced reduction of NO production.</div>
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<Abstract><AbstractText>Exposure to airborne particulate pollutants is intimately linked to vascular oxidative stress and inflammatory responses with clinical relevance to atherosclerosis. Particulate matter (PM) has been reported to induce endothelial dysfunction and atherosclerosis. Here, we tested whether ambient ultrafine particles (UFP, diameter <200 nm) modulate eNOS activity in terms of nitric oxide (NO) production via protein S-glutathionylation. Treatment of human aortic endothelial cells (HAEC) with UFP significantly reduced NO production. UFP-mediated reduction in NO production was restored in the presence of JNK inhibitor (SP600125), NADPH oxidase inhibitor (Apocynin), anti-oxidant (N-acetyl cysteine), and superoxide dismutase mimetics (Tempol and MnTMPyP). UFP exposure increased the GSSG/GSH ratio and eNOS S-glutathionylation, whereas over-expression of Glutaredoxin-1 (to inhibit S-glutathionylation) restored UFP-mediated reduction in NO production by nearly 80%. Thus, our findings suggest that eNOS S-glutathionylation is a potential mechanism underlying ambient UFP-induced reduction of NO production.</AbstractText>
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Ambient ultrafine particles reduce endothelial nitric oxide production via S-glutathionylation of eNOS.

Ambient ultrafine particles reduce endothelial nitric oxide production via S-glutathionylation of eNOS.

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