title: Accumulation of VEGFR-2+/CD133+ cells and decreased number and impaired functionality of CD34+/VEGFR-2+ cells in patients with SLE.
abstract: OBJECTIVE
  Inflammation and atherosclerosis are the major causes of cardiovascular disease (CVD) in SLE. Both traditional and disease-specific risk factors contribute to the formation of endothelial dysfunction. Endothelial progenitor cells (EPCs) have the ability to restore endothelial integrity. The aim of this study was to determine whether the number and function of EPCs are altered in SLE.
  
  
  METHODS
  Nineteen patients with SLE and 19 controls were analysed. VEGF receptor-2 (VEGFR-2)(+)/CD133(+) and CD34(+)/VEGFR-2(+) cells were quantified by flow cytometry. EPC differentiation was measured by DiI-acLDL/Lectin I staining. Furthermore, apoptosis, proliferation capacity, migration capacity and clonogenic ability of EPCs were determined.
  
  
  RESULTS
  VEGFR-2(+)/CD133(+) cells were enhanced in SLE [215 (37) vs 122 (11) cells/1 x 10(6) lymphocytes; P = 0.029], whereas the number [106 (13) vs 215 (27) cells/1 x 10(6) lymphocytes; P = 0.002] and the proliferation rate [96% (6%) vs 143% (19%); P = 0.008] of CD34(+)/VEGFR-2(+) cells were decreased compared with controls. Additionally, EPCs in SLE showed an increased apoptosis [7% (1.4%) vs 3% (0.4%); P = 0.004], an impaired differentiation [36 (5) vs 121 (20) cells/mm(2); P < 0.001] and a reduced migratory capacity [116% (4%) vs 139% (4%); P = 0.001].
  
  
  CONCLUSIONS
  Our results suggest that the mobilization of progenitor cells is unaffected in SLE, but the diminished number and the altered functionality of circulating CD34(+)/VEGFR-2(+) cells reduce the ability to repair vascular damage and thus may trigger the development of atherosclerosis in SLE.
authors.affiliation: Department of Internal Medicine, Division of Cardiology, Pneumology and Angiology, Heinrich-Heine University, Moorenstrasse 5, 40225 Düsseldorf, Germany. petraebner@gmx.de
authors.forename: Petra
authors.initials: P
authors.lastname: Ebner
authors.forename: Frauke
authors.initials: F
authors.lastname: Picard
authors.forename: Jutta
authors.initials: J
authors.lastname: Richter
authors.forename: Eleonore
authors.initials: E
authors.lastname: Darrelmann
authors.forename: Matthias
authors.initials: M
authors.lastname: Schneider
authors.forename: Bodo-Eckehard
authors.initials: BE
authors.lastname: Strauer
authors.forename: Michael
authors.initials: M
authors.lastname: Brehm
mesh_terms: D000071916:AC133 Antigen; D000328:Adult; D015703:Antigens, CD / Q000097:blood; D018952:Antigens, CD34 / Q000097:blood; D017209:Apoptosis / Q000502:physiology; D002318:Cardiovascular Diseases / Q000209:etiology; D002452:Cell Count; D002454:Cell Differentiation / Q000502:physiology; D002465:Cell Movement / Q000502:physiology; D049109:Cell Proliferation; D002478:Cells, Cultured; D003114:Colony-Forming Units Assay; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005260:Female; D006023:Glycoproteins / Q000097:blood; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000150:complications / Q000473:pathology*; D008875:Middle Aged; D010455:Peptides / Q000097:blood; D012307:Risk Factors; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000097:blood
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D006023:Glycoproteins; C000606023:PROM1 protein, human; D010455:Peptides; D040301:Vascular Endothelial Growth Factor Receptor-2