title: Circulating endothelial progenitor cells, vascular function, and cardiovascular risk.
abstract: BACKGROUND
  Cardiovascular risk factors contribute to atherogenesis by inducing endothelial-cell injury and dysfunction. We hypothesized that endothelial progenitor cells derived from bone marrow have a role in ongoing endothelial repair and that impaired mobilization or depletion of these cells contributes to endothelial dysfunction and cardiovascular disease progression.
  
  
  METHODS
  We measured the number of colony-forming units of endothelial progenitor cells in peripheral-blood samples from 45 men (mean [+/-SE] age, 50+/-2 years). The subjects had various degrees of cardiovascular risk but no history of cardiovascular disease. Endothelium-dependent and endothelium-independent function was assessed by high-resolution ultrasonography of the brachial artery.
  
  
  RESULTS
  We observed a strong correlation between the number of circulating endothelial progenitor cells and the subjects' combined Framingham risk factor score (r=-0.47, P=0.001). Measurement of flow-mediated brachial-artery reactivity also revealed a significant relation between endothelial function and the number of progenitor cells (r=0.59, P<0.001). Indeed, the levels of circulating endothelial progenitor cells were a better predictor of vascular reactivity than was the presence or absence of conventional risk factors. In addition, endothelial progenitor cells from subjects at high risk for cardiovascular events had higher rates of in vitro senescence than cells from subjects at low risk.
  
  
  CONCLUSIONS
  In healthy men, levels of endothelial progenitor cells may be a surrogate biologic marker for vascular function and cumulative cardiovascular risk. These findings suggest that endothelial injury in the absence of sufficient circulating progenitor cells may affect the progression of cardiovascular disease.
authors.affiliation: Cardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1622, USA.
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Hill
authors.forename: Gloria
authors.initials: G
authors.lastname: Zalos
authors.forename: Julian P J
authors.initials: JP
authors.lastname: Halcox
authors.forename: William H
authors.initials: WH
authors.lastname: Schenke
authors.forename: Myron A
authors.initials: MA
authors.lastname: Waclawiw
authors.forename: Arshed A
authors.initials: AA
authors.lastname: Quyyumi
authors.forename: Toren
authors.initials: T
authors.lastname: Finkel
mesh_terms: D000328:Adult; D001916:Brachial Artery / Q000502:physiology; D002318:Cardiovascular Diseases; D016922:Cellular Senescence; D003114:Colony-Forming Units Assay; D004730:Endothelium, Vascular / Q000166:cytology* / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012307:Risk Factors; D013234:Stem Cells / Q000502:physiology