title: Number of endothelial progenitor cells in peripheral artery disease as a marker of severity and association with pentraxin-3, malondialdehyde-modified low-density lipoprotein and membrane type-1 matrix metalloproteinase.
abstract: OBJECTIVE
  Circulating endothelial progenitor cells (EPCs) were mobilized in cardiac ischemia, heart failure and vascular injuries associated with endothelial damage. Despite the occurrence of endothelial dysfunction in peripheral artery disease (PAD), few data are available on EPC mobilization in this setting.
  
  
  METHODS
  We investigated the correlations between EPC and disease severity and also other biomarkers in PAD. EPCs assessed as CD34(+) cells co-expressing CD45(dim), CD133 and vascular endothelial growth factor receptor-2 were studied in PAD (n =48) and non-PAD (n =22) patients. Membrane type-1 matrix metalloproteinase (MT1-MMP) on peripheral blood mononuclear cells, serum malondialdehyde-modified low-density lipoprotein (MDA-LDL) and plasma pentraxin-3 were also measured.
  
  
  RESULTS
  The EPC level changed in the Fontaine and Trans-Atlantic Inter-Society Consensus (TASC) II classification. EPC was increased in Fontaine class IIa as compared with class IV and non-PAD patients (p < 0.05). EPCs and pentraxin-3 were increased in TASC II type A/B as compared with type C/D and non-PAD patients (p < 0.05), whereas the expression of MT1-MMP on peripheral blood mononuclear cells was significantly decreased in TASC II type A/B (both p < 0.05 versus type C/D and non-PAD patients). The EPC level showed a positive association with pentraxin-3 (r = 0.31; p < 0.05). There was an inverse association between the EPC level and MT1-MMP (r = -0.54; p < 0.01). The cardiovascular events was associated with reduced EPC and increased MDA-LDL (p < 0.05).
  
  
  CONCLUSIONS
  EPC changed according to the Fontaine and TASC II classification and decreased in the advanced phases, and was associated with novel biomarkers and related to the severity of PAD.
authors: Department of Cardiovascular Medicine, University of Fukui Hospital, Matsuoka, Fukui, Japan.
authors: Tetsuji
authors: T
authors: Morishita
authors: Hiroyasu
authors: H
authors: Uzui
authors: Akira
authors: A
authors: Nakano
authors: Yasuhiko
authors: Y
authors: Mitsuke
authors: Toru
authors: T
authors: Geshi
authors: Takanori
authors: T
authors: Ueda
authors: Jong-Dae
authors: JD
authors: Lee
mesh_terms: D000368:Aged; D018952:Antigens, CD34 / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism*; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000031:analogs & derivatives* / Q000378:metabolism; D053511:Matrix Metalloproteinase 14 / Q000378:metabolism*; D058729:Peripheral Arterial Disease / Q000097:blood / Q000378:metabolism* / Q000473:pathology*; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology*; D000099153:Pentraxins
chemical_list: D018952:Antigens, CD34; D015415:Biomarkers; D002097:C-Reactive Protein; D008077:Lipoproteins, LDL; D008315:Malondialdehyde; D053511:Matrix Metalloproteinase 14; D000683:Serum Amyloid P-Component; D000099153:Pentraxins; C569869:malondialdehyde-low density lipoprotein, human; C507086:MMP14 protein, human