title: Systemic lupus erythematosus patients exhibit functional deficiencies of endothelial progenitor cells.
abstract: OBJECTIVE
  SLE is characterized by an increased cardiovascular risk. Since endothelial progenitor cells (EPCs) have been described to serve as a biomarker for the CV risk and are known to be depleted in various diseases, we were interested if SLE would also be associated with altered peripheral EPC levels or functional abnormalities of these cells.
  
  
  METHODS
  EPCs were quantified in 31 female SLE patients with different disease activity and in age-matched healthy controls (HCs) by FACS analysis and by colony forming unit (CFU) assay. Furthermore, EPC adhesion and migration capacity were tested.
  
  
  RESULTS
  EPC levels were similar in HC and SLE when assessed by FACS (0.045 +/- 0.006% vs 0.036 +/- 0.007% within the lymphocyte gate) and by the CFU assay (18 +/- 3 vs 15 +/- 2 colonies/well). No correlation with disease activity could be observed, but SLE patients treated with chloroquine exhibited significantly decreased EPC levels (0.058 +/- 0.005% without vs 0.024 +/- 0.008% with chloroquine, P < 0.05). Addition of chloroquine to in vitro cultures also led to a decreased colony formation in SLE and in HC. When testing the adhesion and migration capacity of EPC on human umbilical vein endothelial cells (HUVEC), cells from SLE patients had reduced adhesion (19.2 +/- 3.5% vs 36.6 +/- 5.2% EPC/high power field, P < 0.02) and migratory activity (56 +/- 6 cells/random microscopic field in SLE vs 121 +/- 28 in controls, P < 0.02).
  
  
  CONCLUSIONS
  The data reveal that EPCs are significantly affected in SLE. While circulating EPC levels are in the range of HC, they exhibit functional deficiencies that may lead to impaired tissue availability.
authors.affiliation: Department of Internal Medicine III, Division of Rheumatology, Ludwig Boltzmann Institute for Rheumatology and Balneology, Vienna, Austria. johannes.grisar@meduniwien.ac.at
authors.forename: J
authors.initials: J
authors.lastname: Grisar
authors.forename: C W
authors.initials: CW
authors.lastname: Steiner
authors.forename: M
authors.initials: M
authors.lastname: Bonelli
authors.forename: T
authors.initials: T
authors.lastname: Karonitsch
authors.forename: I
authors.initials: I
authors.lastname: Schwarzinger
authors.forename: G
authors.initials: G
authors.lastname: Weigel
authors.forename: G
authors.initials: G
authors.lastname: Steiner
authors.forename: J S
authors.initials: JS
authors.lastname: Smolen
mesh_terms: D000328:Adult; D018501:Antirheumatic Agents / Q000627:therapeutic use; D002448:Cell Adhesion; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D002738:Chloroquine / Q000627:therapeutic use; D016207:Cytokines / Q000097:blood; D042783:Endothelial Cells / Q000502:physiology; D004730:Endothelium, Vascular / Q000473:pathology; D005260:Female; D006133:Growth Substances / Q000097:blood; D006412:Hematopoietic Stem Cells / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000188:drug therapy; D018613:Microscopy, Confocal
chemical_list: D018501:Antirheumatic Agents; D016207:Cytokines; D006133:Growth Substances; D002738:Chloroquine