Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures

Oren M. Tepper, Robert D. Galiano, Jennifer M. Capla, Christoph Kalka, Paul J. Gagne, Glen R. Jacobowitz, Jamie P. Levine, Geoffrey C. Gurtner

Research output: Contribution to journalArticle

1201 Citations (Scopus)

Abstract

Background - 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. Methods and Results - 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% (P<0.01) and inversely correlated with patient levels of hemoglobin A1C (P<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) (P<0.05). In a Matrigel assay, diabetic EPCs were 2.5 times less likely to participate in tubule formation compared with controls (P<0.05). Conclusions - 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.

Original languageEnglish (US)
Pages (from-to)2781-2786
Number of pages6
JournalCirculation
Volume106
Issue number22
DOIs
StatePublished - Nov 26 2002
Externally publishedYes

Fingerprint

Blood Vessels
Endothelial Progenitor Cells
Human Umbilical Vein Endothelial Cells
Diabetes Complications
Growth
Fibronectins
Type 2 Diabetes Mellitus
Cell Biology
Collagen
Endothelial Cells
Tumor Necrosis Factor-alpha
Morbidity
Mortality

Keywords

  • Angiogenesis
  • Collateral circulation
  • Diabetes mellitus

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures. / Tepper, Oren M.; Galiano, Robert D.; Capla, Jennifer M.; Kalka, Christoph; Gagne, Paul J.; Jacobowitz, Glen R.; Levine, Jamie P.; Gurtner, Geoffrey C.

In: Circulation, Vol. 106, No. 22, 26.11.2002, p. 2781-2786.

Research output: Contribution to journalArticle

Tepper, Oren M. ; Galiano, Robert D. ; Capla, Jennifer M. ; Kalka, Christoph ; Gagne, Paul J. ; Jacobowitz, Glen R. ; Levine, Jamie P. ; Gurtner, Geoffrey C. / Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures. In: Circulation. 2002 ; Vol. 106, No. 22. pp. 2781-2786.
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AU - Gagne, Paul J.

AU - Jacobowitz, Glen R.

AU - Levine, Jamie P.

AU - Gurtner, Geoffrey C.

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N2 - Background - 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. Methods and Results - 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% (P<0.01) and inversely correlated with patient levels of hemoglobin A1C (P<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) (P<0.05). In a Matrigel assay, diabetic EPCs were 2.5 times less likely to participate in tubule formation compared with controls (P<0.05). Conclusions - 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.

AB - Background - 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. Methods and Results - 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% (P<0.01) and inversely correlated with patient levels of hemoglobin A1C (P<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) (P<0.05). In a Matrigel assay, diabetic EPCs were 2.5 times less likely to participate in tubule formation compared with controls (P<0.05). Conclusions - 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.

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