A Study of Vascular Wound Healing in a Rabbit Model of Type I Diabetes

  • Natalie K. Schiller
  • Donald L. Akers
  • Brian Burke
  • Alvin M. Timothy
  • Brenda Bedi
  • Dennis B. McNamara
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 498)


The pathophysiology of restenosis following balloon catheterization involves a sequence of events similar to wound healing (1). Mechanical stress and mitogens released by cells at the site of injury activate quiescent vascular smooth muscle cells (VSMC) of the contractile phenotype to dedifferentiate to the synthetic phenotype and, subsequently, divide. Activated VSMC of the synthetic phenotype migrate through breaks in the internal elastic lamina to the intima where they continue to proliferate and synthesize abundant extracellular matrix (ECM), resulting in an increased neointimal mass. This intimal hyperplasia has been suggested to contribute to a decrease in lumen diameter and patency of the vessel resulting in ischemic symptoms. It should be noted, however, that the contribution of intimal thickening to the pathophysiology of restenosis has recently been questioned.


Vascular Smooth Muscle Cell Proliferate Cell Nuclear Antigen Diabetic Animal Vascular Smooth Muscle Cell Proliferation Mitogen Activate Protein Kinase Activity 
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Copyright information

© Springer Science+Business Media New York 2001

Authors and Affiliations

  • Natalie K. Schiller
    • 1
  • Donald L. Akers
    • 1
  • Brian Burke
    • 1
  • Alvin M. Timothy
    • 1
  • Brenda Bedi
    • 1
  • Dennis B. McNamara
    • 1
  1. 1.Departments of Pharmacology and SurgeryTulane University School of MedicineNew OrleansUSA

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