title: Effect of smoking cessation on the number and adhesive properties of early outgrowth endothelial progenitor cells.
abstract: BACKGROUND
  Endothelial progenitor cells participate in angiogenesis and vascular repair, and cardiovascular risk factors may reduce their numbers or impair their functional properties. Cigarette smoking is a leading cause of preventable cardiovascular death, however, the functional properties of these cells before and after discontinuation of tobacco use have not been systematically analyzed.
  
  
  METHODS
  We examined changes in the number and function of early outgrowth endothelial progenitor cells (EPC), isolated from individuals (n=144; mean age, 47.8 ± 12.0 years; 43% males; more than 50% with additional cardiovascular risk factors or disease) who successfully completed a 5-week smoking cessation (SC) programme.
  
  
  RESULTS
  SC significantly reduced total white blood cell count (WBC; P<0.0001), plasma LDL cholesterol (P=0.0002) and fibrinogen (P<0.0001) levels, but did not alter the number of circulating CD34(+), VEGFR2(+) or CD34(+), CD133(+) cells (P=0.14 and 0.57, respectively). Fewer acLDL(+), lectin(+) cells could be expanded from peripheral blood mononuclear cells in comparison to baseline (P<0.001). Furthermore, SC was associated with reduced EPC adhesion to fibronectin (P<0.001) or TNFα-activated endothelial cells (P=0.003), and a diminished incorporation of EPC into endothelial cell networks (P=0.035). Mechanistically, significantly reduced β1- and β2-integrin expression (P<0.001 and 0.007) and lower contents of intracellular reactive oxygen species (P<0.007) were detected in EPC following SC, in addition to reduced plasma asymmetric dimethyl-L-arginine (ADMA) levels (P=0.0003).
  
  
  CONCLUSIONS
  Our findings suggest that the oxidative and inflammatory stress reduction associated with smoking cessation impair the adhesiveness of monocyte-derived EPC.
authors.affiliation: Department of Cardiology and Pulmonary Medicine, Georg August University of Goettingen, Goettingen, Germany.
authors.forename: Miriam
authors.initials: M
authors.lastname: Puls
authors.forename: Marco R
authors.initials: MR
authors.lastname: Schroeter
authors.forename: Jasmin
authors.initials: J
authors.lastname: Steier
authors.forename: Lena
authors.initials: L
authors.lastname: Stijohann
authors.forename: Gerd
authors.initials: G
authors.lastname: Hasenfuss
authors.forename: Stavros
authors.initials: S
authors.lastname: Konstantinides
authors.forename: Katrin
authors.initials: K
authors.lastname: Schäfer
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000453:epidemiology / Q000473:pathology* / Q000503:physiopathology; D015415:Biomarkers / Q000378:metabolism; D018821:CD18 Antigens / Q000378:metabolism; D002448:Cell Adhesion / Q000502:physiology*; D002450:Cell Communication / Q000502:physiology; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005353:Fibronectins / Q000378:metabolism; D006801:Humans; D019012:Integrin beta1 / Q000378:metabolism; D037102:Lectins / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D017382:Reactive Oxygen Species / Q000378:metabolism; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects / Q000453:epidemiology; D016540:Smoking Cessation / Q000706:statistics & numerical data; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology*; D014657:Vasculitis / Q000453:epidemiology / Q000473:pathology* / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D018821:CD18 Antigens; D005353:Fibronectins; D019012:Integrin beta1; D037102:Lectins; D008077:Lipoproteins, LDL; D017382:Reactive Oxygen Species