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Deficiency in number and activity of circulating endothelial progenitor cells (EPCs) is associated with reduced arterial elasticity in humans. Smoking contributes to deterioration in endothelial function and maintenance of cardiovascular homoeostasis. Here, we investigated whether smoke reduced to decline in number and activity of circulating EPCs and the underlying mechanism.
In a cross-sectional study, the number and activity of circulating EPCs as well as branchial-ankle pulse wave velocity (baPWV) of smokers and nonsmokers in healthy subjects were studied. We measured nitric oxide (NO), vascular endothelial growth factors (VEGF) and granulocyte macrophage colony stimulating factor (GM-CSF) levels of plasma and cultured EPCs in smoke-habited and healthy subjects. Then we observed the correlation of on circulating EPCs and baPWV in smokers and nonsmokers respectively.
In all included men, the number and activity of circulating EPCs were significantly low in smokers compared with nonsmokers, which was paralleled to increased baPWV. After three months of smoke cessation, the number and activity of circulating EPCs increased in previous smokers, and the baPWV decreased, combined with increased NO-VEGF level in both plasma and cultured EPCs, but not GM-CSF. There was a close correlation between circulating EPCs and baPWV,and also the circulating EPCs function and NO-VEGF level.
The present study demonstrates for smoke-induced decreased circulating EPCs attenuates the decline in arterial elasticity in healthy men, and smoke cessation would reverse this phenomenon via NO production.