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Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
Published on: January 16, 2015
Increased Rho-kinase expression and activity and pulmonary endothelial dysfunction in smokers with normal lung
S Duong-Quy1, P Dao, T Hua-Huy
1Service de Physiologie - Explorations Fonctionnelles, Hôpital Cochin, 27 rue du Faubourg, Saint-Jacques, 75104 Paris, France.
The European Respiratory Journal
|June 10, 2010
Summary
Cigarette smoking impairs pulmonary artery function even in individuals with normal lung function, affecting endothelial nitric oxide synthase (eNOS) activity and increasing RhoA/ROCK signaling.
Area of Science:
- Cardiovascular Research
- Pulmonary Medicine
- Vascular Biology
Background:
- Cigarette smoke induces endothelial dysfunction.
- The RhoA/ROCK pathway is implicated in smoking-related vascular damage.
Purpose of the Study:
- To investigate the RhoA/ROCK pathway's role in pulmonary artery endothelial function in smokers with normal lung function.
Main Methods:
- Pulmonary artery rings from smokers and nonsmokers were analyzed.
- Vascular relaxation to acetylcholine was measured.
- Protein expression and activity of eNOS, RhoA, ROCKs, and MYPT-1 were assessed.
Main Results:
- Smokers exhibited reduced arterial relaxation and lower eNOS activity compared to nonsmokers.
- eNOS protein levels were unchanged.
- ROCKs, GTP-RhoA, and phosphorylated MYPT-1 levels were elevated in smokers.
Conclusions:
- Pulmonary endothelial dysfunction exists in smokers before lung function decline.
- Reduced eNOS activity and increased RhoA/ROCK pathway signaling contribute to this dysfunction and sustained vasoconstriction.
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