title: Decreased in the number and function of circulation endothelial progenitor cells in patients with avascular necrosis of the femoral head.
abstract: BACKGROUND
  Once non-traumatic avascular necrosis of the femoral head (ANFH) happened, vascular impairment and feeble collateral circulation are followed by poor outcomes. Circulating endothelial progenitor cells (EPCs) may substantially contribute to vascular homeostasis such as vascular repair and new blood vessel growth. We investigated whether abnormalities in EPCs levels and functions are present in ANFH patients.
  
  
  METHODS
  54 ANFH patients were enrolled, including steroid-induced (n=21), alcohol-induced (n=15) and idiopathic ANFH (n=18), and 30 healthy subjects as control (HC). The numbers of circulation EPCs were determined by fluorescence-activated cell-sorting (FACS) analysis. EPCs cultured from peripheral blood mononuclear cells on fibronectin to induce the expression of receptors for acetylated low-density lipoprotein and ulex-lectin. EPCs colony-forming units (CFUs) were observed from 54 patients and 30 healthy controls. Migratory capacity to chemo-attractants (vascular endothelial growth factor) cellular senescence levels and in vitro angiogenesis ability were assessed in age-matched subjects (n=10 per groups).
  
  
  RESULTS
  Mean numbers of circulating EPC were 1460+/-265 cells/ml in HC, 545+/-177 in ANFH, (P<0.001). Mean numbers of CFUs were 26.2+/-6.2 in HC, 19.6+/-7.7 in ANFH,(P<0.001). Although there were not significant differences in circulating EPC and CFUs among the steroid-induced, alcohol-induced or idiopathic three groups, all these risk factors contributed to the decreased circulating EPCs numbers and CFUs. In addition, EPCs from ANFH patients showed reduced migratory capacity and increased cellular senescence compared with EPCs from normal subjects, furthermore the ability of angiogenesis in vitro was also impaired.
  
  
  CONCLUSIONS
  Circulating endothelial progenitor cells (EPCs) numbers and functions are reduced in ANFH patients, suggesting that risk factors of ANFH may alter EPCs biology in angiogenesis and vascular repair.
authors.affiliation: Department of Orthopedics, Union Hospital, Huazhong University of Science and Technology, Wuhan, 430022, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Feng
authors.forename: Shu-Hua
authors.initials: SH
authors.lastname: Yang
authors.forename: Bao-Jun
authors.initials: BJ
authors.lastname: Xiao
authors.forename: Wei-Hua
authors.initials: WH
authors.lastname: Xu
authors.forename: Shu-Nan
authors.initials: SN
authors.lastname: Ye
authors.forename: Tian
authors.initials: T
authors.lastname: Xia
authors.forename: Dong
authors.initials: D
authors.lastname: Zheng
authors.forename: Xian-Zhe
authors.initials: XZ
authors.lastname: Liu
authors.forename: Yun-Fei
authors.initials: YF
authors.lastname: Liao
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D002465:Cell Movement / Q000502:physiology; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000502:physiology; D042783:Endothelial Cells / Q000473:pathology* / Q000502:physiology*; D005260:Female; D005271:Femur Head Necrosis / Q000473:pathology* / Q000503:physiopathology; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D008858:Microscopy, Phase-Contrast; D008875:Middle Aged; D018919:Neovascularization, Physiologic / Q000502:physiology; D013234:Stem Cells / Q000473:pathology* / Q000502:physiology