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Is arginase a potential drug target in tobacco-induced pulmonary endothelial dysfunction?

Priscilla Henno, Christelle Maurey, Françoise Le Pimpec-Barthes, Philippe Devillier, Christophe Delclaux, Dominique Israël-Biet
European Respiratory Journal 2015 46: PA4904; DOI: 10.1183/13993003.congress-2015.PA4904
Priscilla Henno
1Sorbonne Universités, UPMC Université Paris 06, AP-HP, Hôpital Saint Antoine, Département Physiologie-Algologie-Somnologie, Unité Fonctionnelle de Somnologie et Fonction Respiratoire, Paris, France
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Christelle Maurey
1Sorbonne Universités, UPMC Université Paris 06, AP-HP, Hôpital Saint Antoine, Département Physiologie-Algologie-Somnologie, Unité Fonctionnelle de Somnologie et Fonction Respiratoire, Paris, France
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Françoise Le Pimpec-Barthes
1Sorbonne Universités, UPMC Université Paris 06, AP-HP, Hôpital Saint Antoine, Département Physiologie-Algologie-Somnologie, Unité Fonctionnelle de Somnologie et Fonction Respiratoire, Paris, France
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Philippe Devillier
1Sorbonne Universités, UPMC Université Paris 06, AP-HP, Hôpital Saint Antoine, Département Physiologie-Algologie-Somnologie, Unité Fonctionnelle de Somnologie et Fonction Respiratoire, Paris, France
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Christophe Delclaux
1Sorbonne Universités, UPMC Université Paris 06, AP-HP, Hôpital Saint Antoine, Département Physiologie-Algologie-Somnologie, Unité Fonctionnelle de Somnologie et Fonction Respiratoire, Paris, France
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Dominique Israël-Biet
2UPRES EA 220, Hôpital Foch, Suresnes, France
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Abstract

Background: Tobacco-induced pulmonary vascular disease is partly driven by endothelial dysfunction. The bioavailability of NO depends on competition between NOS3 and arginases for their common substrate (L-arginine). We tested the hypothesis whereby tobacco smoking impairs pulmonary endothelial function via upregulation of the arginase pathway.

Methods: Endothelium-dependent vasodilation in response to acetylcholine (Ach) was compared ex vivo for pulmonary vascular rings from 29 smokers and 10 never-smokers. We tested the effects of L-arginine supplementation, arginase inhibition (by NorNOHA) and NOS3 induction (by genistein) on vasodilation. Protein levels of NOS3, arginases I and II in the pulmonary arteries were quantified by Western blotting.

Results: Overall, vasodilation was impaired in smokers (relative to controls; p<0.01). Eleven of the 29 smokers (the ED+ subgroup) displayed endothelial dysfunction (defined as the absence of a relaxant response to Ach), whereas 18 (the ED- subgroup) had normal vasodilation (-23±10% vs 31±4% at Ach 10-4M in the ED+ and ED- subgroups, respectively, p<0.01). Supplementation with L- arginine improved endothelial function in the ED+ subgroup (-4±10% vs. -32±10% in the presence and absence of L- arginine, respectively; p=0.006), as did arginase inhibition (18±9% vs. -1±9%, respectively; p=0.0002). Arginase I protein was overexpressed in ED+ samples, whereas ED+ and ED- samples did not differ significantly in terms of NOS3 expression. Genistein did not improve endothelial function in ED+ samples.

Conclusion: Overexpression and elevated activity of arginase I are involved in tobacco-induced pulmonary endothelial dysfunction.

  • COPD - mechanism
  • Smoking
  • Nitric oxide
  • Copyright ©ERS 2015
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Is arginase a potential drug target in tobacco-induced pulmonary endothelial dysfunction?
Priscilla Henno, Christelle Maurey, Françoise Le Pimpec-Barthes, Philippe Devillier, Christophe Delclaux, Dominique Israël-Biet
European Respiratory Journal Sep 2015, 46 (suppl 59) PA4904; DOI: 10.1183/13993003.congress-2015.PA4904

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Is arginase a potential drug target in tobacco-induced pulmonary endothelial dysfunction?
Priscilla Henno, Christelle Maurey, Françoise Le Pimpec-Barthes, Philippe Devillier, Christophe Delclaux, Dominique Israël-Biet
European Respiratory Journal Sep 2015, 46 (suppl 59) PA4904; DOI: 10.1183/13993003.congress-2015.PA4904
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