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1.
Experimental & Molecular Medicine ; : 594-602, 2012.
Article Dans Anglais | WPRIM | ID: wpr-14963

Résumé

The incidence of cardiovascular disease is predicted to increase as the population ages. There is accumulating evidence that arginase upregulation is associated with impaired endothelial function. Here, we demonstrate that arginase II (ArgII) is upregulated in aortic vessels of aged mice and contributes to decreased nitric oxide (NO) generation and increased reactive oxygen species (ROS) production via endothelial nitric oxide synthase (eNOS) uncoupling. Inhibiting ArgII with small interfering RNA technique restored eNOS coupling to that observed in young mice and increased NO generation and decreased ROS production. Furthermore, enhanced vasoconstrictor responses to U46619 and attenuated vasorelaxation responses to acetylcholine in aged vasculature were markedly improved following siRNA treatment against ArgII. These results might be associated with increased L-arginine bioavailability. Collectively, these results suggest that ArgII may be a valuable target in age-dependent vascular diseases.


Sujets)
Animaux , Souris , Acide 15-hydroxy-11alpha,9alpha-(époxyméthano)prosta-5,13-diénoïque/pharmacologie , Vieillissement , Aorte/enzymologie , Arginase/génétique , Endothélium vasculaire/enzymologie , Induction enzymatique , Techniques de knock-down de gènes , Souris de lignée C57BL , Monoxyde d'azote/métabolisme , Nitric oxide synthase type III/métabolisme , Petit ARN interférent/génétique , Espèces réactives de l'oxygène/métabolisme , Régulation positive , Vasoconstriction/effets des médicaments et des substances chimiques
2.
Korean Journal of Anesthesiology ; : 3-11, 2011.
Article Dans Anglais | WPRIM | ID: wpr-171796

Résumé

Atherosclerotic vascular disease is the leading cause of morbidity and mortality in developed countries. While it is a complex condition resulting from numerous genetic and environmental factors, it is well recognized that oxidized low-density lipoprotein produces pro-atherogenic effects in endothelial cells (ECs) by inducing the expression of adhesion molecules, stimulating EC apoptosis, inducing superoxide anion formation and impairing protective endothelial nitric oxide (NO) formation. Emerging evidence suggests that the enzyme arginase reciprocally regulates NO synthase and NO production by competing for the common substrate L-arginine. As oxidized LDL (OxLDL) results in arginase activation/upregulation, it appears to be an important contributor to endothelial dysfunction by a mechanism that involves substrate limitation for endothelial NO synthase (eNOS) and NO synthesis. Additionally, arginase enhances production of reactive oxygen species by eNOS. Arginase inhibition in hypercholesterolemic (ApoE-/-) mice or arginase II deletion (ArgII-/-) mice restores endothelial vasorelaxant function, reduces vascular stiffness and markedly reduces atherosclerotic plaque burden. Furthermore, arginase activation contributes to vascular changes including polyamine-dependent vascular smooth muscle cell proliferation and collagen synthesis. Collectively, arginase may play a key role in the prevention and treatment of atherosclerotic vascular disease.


Sujets)
Animaux , Souris , Apoptose , Arginase , Arginine , Athérosclérose , Prolifération cellulaire , Collagène , Pays développés , Cellules endothéliales , Lipoprotéines , Lipoprotéines LDL , Muscles lisses vasculaires , Monoxyde d'azote , Nitric oxide synthase , Nitric oxide synthase type III , Plaque d'athérosclérose , Espèces réactives de l'oxygène , Superoxydes , Maladies vasculaires , Rigidité vasculaire
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