Human Endothelial Progenitor Cells From Type II Diabetics Exhibit Impaired Proliferation, Adhesion, and Incorporation Into Vascular Structures

DOI Web Site 46 Citations
  • Oren M. Tepper
    From the Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY (O.M.T., R.D.G., J.M.C., J.P.L., G.C.G.); the Department of Cardiology, Pneumology, and Vascular Medicine, Heinrich-Heine University, Duesseldorf, Germany (C.K.); and the Department of Surgery, New York University Medical Center, New York, NY (P.J.G., G.R.J.).
  • Robert D. Galiano
    From the Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY (O.M.T., R.D.G., J.M.C., J.P.L., G.C.G.); the Department of Cardiology, Pneumology, and Vascular Medicine, Heinrich-Heine University, Duesseldorf, Germany (C.K.); and the Department of Surgery, New York University Medical Center, New York, NY (P.J.G., G.R.J.).
  • Jennifer M. Capla
    From the Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY (O.M.T., R.D.G., J.M.C., J.P.L., G.C.G.); the Department of Cardiology, Pneumology, and Vascular Medicine, Heinrich-Heine University, Duesseldorf, Germany (C.K.); and the Department of Surgery, New York University Medical Center, New York, NY (P.J.G., G.R.J.).
  • Christoph Kalka
    From the Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY (O.M.T., R.D.G., J.M.C., J.P.L., G.C.G.); the Department of Cardiology, Pneumology, and Vascular Medicine, Heinrich-Heine University, Duesseldorf, Germany (C.K.); and the Department of Surgery, New York University Medical Center, New York, NY (P.J.G., G.R.J.).
  • Paul J. Gagne
    From the Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY (O.M.T., R.D.G., J.M.C., J.P.L., G.C.G.); the Department of Cardiology, Pneumology, and Vascular Medicine, Heinrich-Heine University, Duesseldorf, Germany (C.K.); and the Department of Surgery, New York University Medical Center, New York, NY (P.J.G., G.R.J.).
  • Glen R. Jacobowitz
    From the Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY (O.M.T., R.D.G., J.M.C., J.P.L., G.C.G.); the Department of Cardiology, Pneumology, and Vascular Medicine, Heinrich-Heine University, Duesseldorf, Germany (C.K.); and the Department of Surgery, New York University Medical Center, New York, NY (P.J.G., G.R.J.).
  • Jamie P. Levine
    From the Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY (O.M.T., R.D.G., J.M.C., J.P.L., G.C.G.); the Department of Cardiology, Pneumology, and Vascular Medicine, Heinrich-Heine University, Duesseldorf, Germany (C.K.); and the Department of Surgery, New York University Medical Center, New York, NY (P.J.G., G.R.J.).
  • Geoffrey C. Gurtner
    From the Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY (O.M.T., R.D.G., J.M.C., J.P.L., G.C.G.); the Department of Cardiology, Pneumology, and Vascular Medicine, Heinrich-Heine University, Duesseldorf, Germany (C.K.); and the Department of Surgery, New York University Medical Center, New York, NY (P.J.G., G.R.J.).

Abstract

<jats:p><jats:bold><jats:italic>Background—</jats:italic></jats:bold>The recent discovery of circulating endothelial progenitor cells (EPCs) has altered our understanding of new blood vessel growth such as occurs during collateral formation. Because diabetic complications occur in conditions in which EPC contributions have been demonstrated, EPC dysfunction may be important in their pathophysiology.</jats:p><jats:p><jats:bold><jats:italic>Methods and Results—</jats:italic></jats:bold>EPCs were isolated from human type II diabetics (n=20) and age-matched control subjects (n=20). Proliferation of diabetic EPCs relative to control subjects was decreased by 48% (<jats:italic>P</jats:italic><0.01) and inversely correlated with patient levels of hemoglobin A1C (<jats:italic>P</jats:italic><0.05). Diabetic EPCs had normal adhesion to fibronectin, collagen, and quiescent endothelial cells but a decreased adherence to human umbilical vein endothelial cells activated by tumor necrosis factor-α (TNF-α) (<jats:italic>P</jats:italic><0.05). In a Matrigel assay, diabetic EPCs were 2.5 times less likely to participate in tubule formation compared with controls (<jats:italic>P</jats:italic><0.05).</jats:p><jats:p><jats:bold><jats:italic>Conclusions—</jats:italic></jats:bold>These findings suggest that type II diabetes may alter EPC biology in processes critical for new blood vessel growth and may identify a population at high risk for morbidity and mortality after vascular occlusive events.</jats:p>

Journal

  • Circulation

    Circulation 106 (22), 2781-2786, 2002-11-26

    Ovid Technologies (Wolters Kluwer Health)

Citations (46)*help

See more

Keywords

Details 詳細情報について

Report a problem

Back to top