Smoking-induced monocyte dysfunction is reversed by vitamin C supplementation in vivo
Research output: Contribution to journal › Research article › Contributed › peer-review
Contributors
Abstract
OBJECTIVE: The role of antioxidants in preventing vascular disease remains controversial. Vascular endothelial growth factor (VEGF-A) is important for endothelial and monocyte function. This study investigated the negative effects of smoking on monocyte migratory responsiveness to VEGF-A and the usefulness of vitamin C to prevent smoking-induced monocyte dysfunction.
METHODS AND RESULTS: The chemotactic response of isolated monocytes from a cohort of 17 non-smokers and 10 smokers toward VEGF-A was assessed. VEGF-A significantly stimulated the migration of monocytes in non-smokers; the monocytes from smokers failed to respond to VEGF-A. Repeated analysis after 2 weeks of vitamin C intake (2 g/d) showed a fully restored VEGF-A-induced monocyte migration in smokers. VEGF-A serum levels were not altered by vitamin C. VEGF-A-inducible kinase activity was intact in monocytes from smokers as assessed by in vitro kinase assay. Monocyte dysfunction can be mimicked in vitro by challenging monocytes with a range of reactive oxygen species (ROS).
CONCLUSIONS: Stimulation of monocyte migration by VEGF-A was severely attenuated in smokers, and the deficit observed was surmounted by vitamin C supplementation. The negative effects of smoking on monocyte function may translate into adverse impacts on VEGF-A-dependent repair processes such as arteriogenesis. These results propose a causative role of oxidative stress in smoking-induced monocyte dysfunction.
Details
Original language | English |
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Pages (from-to) | 120-6 |
Number of pages | 7 |
Journal | Arteriosclerosis, thrombosis, and vascular biology |
Volume | 27 |
Issue number | 1 |
Publication status | Published - Jan 2007 |
Peer-reviewed | Yes |
External IDs
Scopus | 33847651710 |
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ORCID | /0000-0002-7481-0220/work/142247422 |
Keywords
Sustainable Development Goals
Keywords
- Adult, Antioxidants/pharmacology, Ascorbic Acid/pharmacology, Cardiovascular Diseases/etiology, Cell Movement/drug effects, Chemotaxis/drug effects, Dietary Supplements, Humans, Male, Monocytes/drug effects, Oxidative Stress/physiology, Reactive Oxygen Species/pharmacology, Risk Factors, Smoking/adverse effects, Vascular Endothelial Growth Factor A/pharmacology