Smoking increases the premature associated senescence phenotype of circulating Endothelial Progenitor Cells

Abstract

Smoking is a risk factor for cardiovascular disease. Notably, it is associated with endothelial progenitor cells (EPCs) dysfunction. It also influences the shift of the EPCs mobilisation from bone marrow. We hypothesized that smoking could induce a premature associated senescence phenotype on the circulating population of EPCs, which may contribute to the default of recovery endothelial injury. Peripheral Blood Mononuclear Cell (PBMC) samples were collected from 30 smokers at least for five years and 31 healthy subjects (non-smoker) as control. CD117+ and CD133+ cells were confirmed as the population of endothelial progenitor cells. Those marked cells with SA-P galactosidase were quantified as senescence phenotype. Then, FACS assessed the targeted cells. The average concentration of CD133+/CD117+ was 0.05% (±0.03) for smoker subjects and 0.03% (±0.02) for non-smoker (p< 0.05). Almost all of the EPCs population (98.33±3.53%) in the smoker group expressed SA-P gal positive cells (p<0.001). Thus, this study suggests that smoking is associated with a significant elevated premature senescence of EPCs, which may contribute to diminished bioavailability of mature EPCs of the smoker, reducing the potency of vascular maintenance and repair.