title: VE-Cadherin(low)α-smooth muscle actin+ component of vascular progenitor cells correlates with the coronary artery Gensini score.
abstract: BACKGROUND
  Vascular progenitor cells (VPCs) are a heterogeneous population, containing a subpopulation co-expressing both endothelial and smooth muscle phenotypes. This study sought to determine whether the level of this subpopulation correlated with the coronary Gensini score.
  
  
  RESULTS
  VPCs were cultivated in 50 patients undergoing coronary angiography. A subpopulation of VPCs expressed both endothelial (VE-cadherin [VE-Cad]) and smooth-muscle phenotypes (α-smooth muscle actin [α-SMA]). Correlations of the VE-Cad(low)α-SMA(+) VPC level and adhesion molecule expression by VPCs with the Gensini score were investigated. The association between the amount of this subpopulation and the development of intimal hyperplasia (IH) was also estimated in a vascular injury animal model. Both the number of VE-Cad(low)α-SMA(+) VPCs (P = 0.002) and the expression level of intracellular adhesion molecule (ICAM)-1 by VPCs (P = 0.008) correlated with the Gensini score. However, only the number of VE-Cad(low)α-SMA(+) VPCs (P = 0.004) and the blood level of low-density lipoprotein cholesterol (P = 0.016) were parameters independently associated with the Gensini score in multivariate analysis. Furthermore, in an animal model of injecting VPCs into SCID mice after femoral artery wire injury, a higher number of VE-Cad(low)α-SMA(+) VPCs correlated with greater IH (r = 0.69, P<0.0001).
  
  
  CONCLUSIONS
  The level of VE-Cad(low)α-SMA(+) VPCs was associated with the severity of coronary atherosclerosis as quantified by the Gensini score. Manipulating this subpopulation may provide a way of attenuating atherosclerosis in the future.
authors: Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan. bearty@adm.cgmh.org.tw
authors: Chao-Hung
authors: CH
authors: Wang
authors: I-Chang
authors: IC
authors: Hsieh
authors: Shih-Jen
authors: SJ
authors: Chen
authors: Jong-Shyan
authors: JS
authors: Wang
authors: Wen-Jin
authors: WJ
authors: Cherng
authors: Chun-Chi
authors: CC
authors: Chen
authors: Iii-Jan
authors: IJ
authors: Lam
authors: Shing-Jong
authors: SJ
authors: Lin
mesh_terms: D000199:Actins / Q000378:metabolism*; D000368:Aged; D000787:Angina Pectoris / Q000378:metabolism / Q000473:pathology; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism*; D015820:Cadherins / Q000378:metabolism*; D002448:Cell Adhesion / Q000502:physiology; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000378:metabolism* / Q000473:pathology; D003331:Coronary Vessels / Q000166:cytology / Q000378:metabolism*; D042783:Endothelial Cells / Q000166:cytology; D005260:Female; D018380:Hematopoietic Stem Cell Transplantation; D006412:Hematopoietic Stem Cells / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D008297:Male; D051379:Mice; D016513:Mice, SCID; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D012720:Severity of Illness Index; D000099152:Cadherin 5
chemical_list: D000199:Actins; D015703:Antigens, CD; D015820:Cadherins; D000099152:Cadherin 5; C541116:ACTA2 protein, human