title: Imbalance between endothelial progenitors cells and microparticles in HIV-infected patients naive for antiretroviral therapy.
abstract: BACKGROUND
  Cardiovascular events have been reported among HIV-infected patients following antiretroviral therapy. However, the role of HIV itself in determining vascular damage is less described. Chronic inflammatory state might impair some regulatory endothelium properties leading to its activation, apoptosis or erosion.
  
  
  OBJECTIVE
  To evaluate the balance between endothelial progenitor cells and microparticles in HIV-infected antiretroviral drug-naive patients.
  
  
  METHODS
  A case-control study comparing HIV-infected patients (n = 35) with sex-matched and age-matched healthy controls (n = 33).
  
  
  METHODS
  Endothelial progenitor cells populations expressing CD34, CD133 and KDR were quantified by flow cytometry. Endothelial-derived microparticles, expressing CD51, and platelet-derived microparticles, expressing CD31/CD42, were also measured. Endothelial function was estimated by flow-mediated dilation.
  
  
  RESULTS
  Lower percentages of endothelial progenitor cells (CD34/KDR) were observed in HIV-infected individuals compared with controls (0.02 vs. 0.09%, P = 0.045). In addition, endothelial microparticles concentration was higher in HIV-infected individuals (1963 vs. 436 microparticles/μl platelet-poor plasma, P = 0.003), with similar number of platelet-derived microparticles among groups. Furthermore, flow-mediated dilation was lower among HIV-infected individuals compared with controls [mean (SEM): 10 (1) and 16% (2), respectively; P = 0.03].
  
  
  CONCLUSIONS
  Our findings suggest an imbalance between endothelial progenitor cells mobilization and endothelial apoptosis. The alteration in the turnover of endothelial cells may contribute to cardiovascular events in HIV-infected patients.
authors.affiliation: Infectious Diseases Division, Federal University of São Paulo, Brazil. erikaferrari@uol.com.br
authors.forename: Erika F R
authors.initials: EF
authors.lastname: da Silva
authors.forename: Francisco A H
authors.initials: FA
authors.lastname: Fonseca
authors.forename: Carolina N
authors.initials: CN
authors.lastname: França
authors.forename: Paulo R A
authors.initials: PR
authors.lastname: Ferreira
authors.forename: Maria C O
authors.initials: MC
authors.lastname: Izar
authors.forename: Reinaldo
authors.initials: R
authors.lastname: Salomão
authors.forename: Luciano M
authors.initials: LM
authors.lastname: Camargo
authors.forename: Simone B
authors.initials: SB
authors.lastname: Tenore
authors.forename: David S
authors.initials: DS
authors.lastname: Lewi
mesh_terms: D000071916:AC133 Antigen; D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D018952:Antigens, CD34 / Q000378:metabolism; D017209:Apoptosis; D001938:Brazil; D016022:Case-Control Studies; D055252:Cell-Derived Microparticles / Q000378:metabolism*; D042783:Endothelial Cells / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D005434:Flow Cytometry; D006023:Glycoproteins / Q000378:metabolism; D015658:HIV Infections / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D039564:Integrin alphaV / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D019038:Platelet Glycoprotein GPIb-IX Complex / Q000378:metabolism; D011446:Prospective Studies; D013234:Stem Cells / Q000378:metabolism*; D014664:Vasodilation; D055815:Young Adult
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D006023:Glycoproteins; D039564:Integrin alphaV; C000606023:PROM1 protein, human; D010455:Peptides; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D019038:Platelet Glycoprotein GPIb-IX Complex