title: Enhanced functional response of CD133+ circulating progenitor cells in patients early after acute myocardial infarction.
abstract: OBJECTIVE
  Circulating progenitor cells (PC) may contribute to myocardial recovery following infarction. Growth factors including VEGF are produced during ischaemia and stimulate PC release and activation. In this study, we focused on the functional chemotactic response of PC to VEGF in subjects early after myocardial ischaemia.
  
  
  RESULTS
  Number and phenotype of PC were characterized using flow-cytometry. CD133(+)PC were isolated from peripheral blood using positive MACS isolation. The chemotactic response towards members of the VEGF family (VEGF-A, PlGF-1, and VEGF-E) was analysed in three groups: (i) early period following acute myocardial infarction (days 2-4) treated with primary PCI (AMI) (n = 35), (ii) stable coronary artery disease (CAD) (n = 35), and (iii) controls (CTR) (n = 20). CD133(+)PC number was 2-fold higher in AMI when compared with CAD and CTR (P = 0.0001), whereas CAD was not different from CTR. The chemotactic response of CD133(+)PC to VEGF-A, PlGF-1, and VEGF-E was significantly enhanced (2-fold) in AMI when compared with CAD (P = 0.0001). While the increase of the VEGFR-1-mediated/PlGF-triggered response was rapid (2 days following infarction), the VEGFR-2-mediated/VEGF-E-triggered response was maximally increased on day 4 post-AMI, thus correlating with the kinetics of maximal inflammatory activation reflected by increased CRP levels (P = 0.019).
  
  
  CONCLUSIONS
  The enhanced chemotactic response of CD133(+)PC following myocardial infarction represents a novel principle potentially involved in cardiovascular repair early after myocardial infarction. Acute inflammatory processes are closely associated with this increased cellular function.
authors.affiliation: Department of Cardiology, University Hospital of Maastricht, P. Debyelaan 25, PO Box 5800, 6202AZ Maastricht, The Netherlands.
authors.forename: Stefan
authors.initials: S
authors.lastname: Vöö
authors.forename: Juliane
authors.initials: J
authors.lastname: Eggermann
authors.forename: Marina
authors.initials: M
authors.lastname: Dunaeva
authors.forename: Carolien
authors.initials: C
authors.lastname: Ramakers-van Oosterhoud
authors.forename: Johannes
authors.initials: J
authors.lastname: Waltenberger
mesh_terms: D000071916:AC133 Antigen; D015703:Antigens, CD / Q000097:blood*; D002453:Cell Cycle; D002633:Chemotaxis / Q000502:physiology*; D003324:Coronary Artery Disease / Q000097:blood; D004812:Epidemiologic Methods; D005260:Female; D005434:Flow Cytometry; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000473:pathology*; D010455:Peptides / Q000097:blood*; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D006023:Glycoproteins; C000606023:PROM1 protein, human; D010455:Peptides; D042461:Vascular Endothelial Growth Factor A; D040281:Vascular Endothelial Growth Factor Receptor-1