title: Decreased number and impaired angiogenic function of endothelial progenitor cells in patients with chronic renal failure.
abstract: OBJECTIVE
  Increased risk of cardiovascular disease in patients with chronic renal failure (CRF) has been explained by accelerated atherosclerosis and impaired angiogenesis, in which endothelial progenitor cells (EPCs) may play key roles. We hypothesized that altered EPC biology may contribute to the pathophysiology of CRF.
  
  
  RESULTS
  EPCs were isolated from CRF patients on maintenance hemodialysis (n=44) and from a normal control group (n=30). CRF patients showed markedly decreased numbers of EPC (44.6%) and colonies (75.3%) when compared with the controls (P<0.001). These findings were corroborated by 30.5% decrease in EPC migratory function in response to vascular endothelial growth factor (VEGF) (P=0.040) and 48.8% decrease in EPC incorporation into human umbilical vein endothelial cells (HUVEC) (P<0.001). In addition, Framingham's risk factor score of both CRF (r=-0.461, P=0.010) and normal group (r=-0.367, P=0.016) significantly correlated with the numbers of EPC. Indeed, the number of circulating EPC was significantly lower in CRF patients than in normal group under the same burden of risk factors (P<0.001). A significant correlation was also observed between dialysis dose (Kt/V) and EPC incorporation into HUVEC (r=0.427, P=0.004).
  
  
  CONCLUSIONS
  EPC biology, which is critical for neovascularization and the maintenance of vascular function, is altered in CRF. Our data strongly suggest that dysfunction of circulating EPC has a role in the progression of cardiovascular disease in patients with CRF.
authors.affiliation: Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
authors.forename: Jin-Ho
authors.initials: JH
authors.lastname: Choi
authors.forename: Koung Li
authors.initials: KL
authors.lastname: Kim
authors.forename: Wooseong
authors.initials: W
authors.lastname: Huh
authors.forename: Beom
authors.initials: B
authors.lastname: Kim
authors.forename: Jonghoe
authors.initials: J
authors.lastname: Byun
authors.forename: Wonhee
authors.initials: W
authors.lastname: Suh
authors.forename: Jidong
authors.initials: J
authors.lastname: Sung
authors.forename: Eun-Seok
authors.initials: ES
authors.lastname: Jeon
authors.forename: Ha-Young
authors.initials: HY
authors.lastname: Oh
authors.forename: Duk-Kyung
authors.initials: DK
authors.lastname: Kim
mesh_terms: D000368:Aged; D002452:Cell Count; D019070:Cell Lineage; D002465:Cell Movement; D002478:Cells, Cultured / Q000473:pathology; D003094:Collagen; D003114:Colony-Forming Units Assay; D003327:Coronary Disease / Q000453:epidemiology; D004338:Drug Combinations; D042783:Endothelial Cells / Q000473:pathology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000473:pathology* / Q000503:physiopathology / Q000628:therapy; D007797:Laminin; D008297:Male; D059630:Mesenchymal Stem Cells / Q000187:drug effects / Q000473:pathology*; D008875:Middle Aged; D009024:Morphogenesis; D009389:Neovascularization, Pathologic / Q000503:physiopathology*; D011509:Proteoglycans; D006435:Renal Dialysis; D012307:Risk Factors; D042461:Vascular Endothelial Growth Factor A / Q000494:pharmacology
chemical_list: D004338:Drug Combinations; D007797:Laminin; D011509:Proteoglycans; D042461:Vascular Endothelial Growth Factor A; C059485:matrigel; D003094:Collagen