title: Endothelial progenitor cells and vascular dysfunction in children with obstructive sleep apnea.
abstract: BACKGROUND
  Endothelial dysfunction is a potential complication of obstructive sleep apnea syndrome (OSAS) in children ascribed to systemic inflammatory changes. However, not all children with OSAS will manifest endothelial dysfunction.
  
  
  OBJECTIVE
  The variability in endothelial function in pediatric OSAS may be related to the ability to recruit repair mechanisms such as endothelial progenitor cells (EPCs).
  
  
  METHODS
  Prepubertal nonhypertensive children with or without polysomonographically confirmed OSAS had endothelial function assessed in a morning fasted state using a modified hyperemic test involving cuff-induced occlusion of the radial and ulnar arteries. Blood was drawn and EPCs were assessed by flow cytometry and triple staining using antibodies against CD133, CD34, and vascular endothelial growth factor receptor-2 after isolation of peripheral blood mononuclear cells. SDF-1 levels were measured by ELISA.
  
  
  RESULTS
  Eighty children with OSAS (mean age 8.2 +/- 1.4 yr, mean body mass index [BMI] z-score, 1.43 +/- 0.3) and 20 controls (CO) matched for BMI, age, sex, and ethnicity were studied. Significant delays to peak capillary reperfusion after occlusion release (Tmax) occurred in OSAS children, but substantial variability was present. Despite similar OSAS severity, EPC counts, and stromal cell-derived factor-1 (SDF-1) levels were significantly lower among the 20 OSAS children with the longest Tmax, when compared with either the 20 children with normal Tmax values or to CO ( P < 0.01). Furthermore, Tmax was significantly and inversely correlated with EPCs (r(2), 0.51; P < 0.01), but neither EPCs nor Tmax were associated with apnea-hyponea index (AHI).
  
  
  CONCLUSIONS
  Endothelial dysfunction is frequently present in OSAS. Variance in endothelial functional phenotype may not only reside in the individual susceptibility but also in the ability to recruit endothelial repair mechanisms.
authors.affiliation: Section of Pediatric Sleep Medicine, Department of Pediatrics, The University of Chicago, 5721 S Maryland Avenue, MC 8000, Suite K-160, Chicago, IL 60637, USA.
authors.forename: Leila
authors.initials: L
authors.lastname: Kheirandish-Gozal
authors.forename: Rakesh
authors.initials: R
authors.lastname: Bhattacharjee
authors.forename: Jinkwan
authors.initials: J
authors.lastname: Kim
authors.forename: Heather B
authors.initials: HB
authors.lastname: Clair
authors.forename: David
authors.initials: D
authors.lastname: Gozal
mesh_terms: D001772:Blood Cell Count; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D054377:Chemokine CXCL12 / Q000097:blood; D002648:Child; D002675:Child, Preschool; D042783:Endothelial Cells / Q000502:physiology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D017286:Polysomnography; D015424:Reperfusion; D020181:Sleep Apnea, Obstructive / Q000097:blood* / Q000503:physiopathology; D013234:Stem Cells
chemical_list: D054377:Chemokine CXCL12; D002097:C-Reactive Protein