title: Endothelial progenitor cells, cardiovascular risk factors, cytokine levels and atherosclerosis--results from a large population-based study.
abstract: BACKGROUND
  EPC number and functionality are assumed to reflect the endogenous vascular repair capacity with the EPC pool declining in higher ages and being exhausted by unfavorable life-style and risk factors. This intriguing and clinically highly relevant concept, however, has so far been derived from small case-control studies and patient series.
  
  
  RESULTS
  In the population-based Bruneck Study EPC number and EPC-colony forming units (EPC-CFU) were assessed as part of the fourth follow-up evaluation (2005) in 571 and 542 subjects, respectively. EPC number declined with age (p = 0.013), was significantly lower in women (p = 0.006) and higher in subjects on statin, hormone replacement or ACE inhibitor/angiotensin-receptor blockers, and correlated positively with moderate alcohol consumption. Unexpectedly, a positive relation between EPC number and several vascular risk factors emerged. In a step forward multivariate linear regression analysis EPC number was independently related with SDF1alpha, MMP-9, triglycerides, alcohol consumption, and Hba1c. EPC-CFU in turn was related to SDF1alpha and diastolic blood pressure. Moreover, EPC number showed a significant positive association with the Framingham risk score (P = 0.001). Finally, there was an inverse association between EPC number and common carotid artery intima-media thickness (p = 0.02) and the carotid artery atherosclerosis score (p = 0.059).
  
  
  CONCLUSIONS
  Our population-based data confirm the decline of EPC number with advancing age and lend first epidemiological support to a role of SDF-1alpha and MMP9 in EPC differentiation, mobilization and homing, but are conflict with the view that EPC number is unfavorably affected by cardiovascular risk factors. EPC number increases with the cardiovascular risk estimated by the Framingham risk score (FRS), which in the absence of similar changes for EPC-CFU. Finally, we demonstrate a significant inverse association between EPC number and extent of carotid atherosclerosis even though this association was only of moderate strength and not entirely consistent in other vascular territories.
authors.affiliation: Cardiovascular Division, King's College London, University of London, London, United Kingdom.
authors.forename: Qingzhong
authors.initials: Q
authors.lastname: Xiao
authors.forename: Stefan
authors.initials: S
authors.lastname: Kiechl
authors.forename: Seema
authors.initials: S
authors.lastname: Patel
authors.forename: Friedrich
authors.initials: F
authors.lastname: Oberhollenzer
authors.forename: Siegfried
authors.initials: S
authors.lastname: Weger
authors.forename: Agnes
authors.initials: A
authors.lastname: Mayr
authors.forename: Bernhard
authors.initials: B
authors.lastname: Metzler
authors.forename: Markus
authors.initials: M
authors.lastname: Reindl
authors.forename: Yanhua
authors.initials: Y
authors.lastname: Hu
authors.forename: Johann
authors.initials: J
authors.lastname: Willeit
authors.forename: Qingbo
authors.initials: Q
authors.lastname: Xu
mesh_terms: D050197:Atherosclerosis / Q000175:diagnosis* / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000175:diagnosis* / Q000378:metabolism; D002339:Carotid Arteries / Q000473:pathology; D054377:Chemokine CXCL12 / Q000096:biosynthesis; D016207:Cytokines / Q000378:metabolism*; D042783:Endothelial Cells / Q000166:cytology*; D004730:Endothelium, Vascular / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D015203:Reproducibility of Results; D012307:Risk Factors; D013234:Stem Cells / Q000166:cytology* / Q000378:metabolism
chemical_list: D054377:Chemokine CXCL12; D016207:Cytokines