Table 1

Summary of targets for gene therapy in animal models of vascular injury

Model Lesion inhibition (%)
Antiproliferative action
 Antisense oligodeoxynucleotide
  c-myb Rat carotid84
  c-myc Porcine coronary70
  PCNARat carotid80
  cyclin BRat carotid60
  cyclin G1 Rat carotid64
  CDK-1Rat carotid40–47
  CDK-2 Rat carotid55–60
  CDK-1 + CDK-2Rat carotid85
  CDK-1 + PCNARat carotid60
  CDK-1 + cyclin BRat carotid78
 Decoy oligodeoxynucleotide
  E2FRat carotid74
 Gene transfer
  pRb (non-phosphorylatable)Rat carotid
Porcine femoral		50
47
  p130Rat carotid81
  p21Cip1 Rat carotid
Porcine femoral		46–58
37
  p27Kip1 Rat carotid49
  p53Rabbit carotid85
  GAXRabbit iliac56
  ras (dominant negative)Rat carotid62
Pro-apoptotic action
 Antisense oligodeoxynucleotide
  bcl-xL Rabbit carotid561-150
 Gene transfer
  Fas-ligandRat carotid60–73
Matrix action
 Gene transfer
  TIMP-1Rat carotid30
Pleiomorphic action
 Gene transfer
  eNOSRat carotid56–72
  iNOSRat carotid95
Porcine iliac52

  • CDK, cyclin dependent kinase; eNOS, endothelial nitric oxide synthase; iNOS, inducible nitric oxide synthase; GAX, growth arrest specific homeobox gene; pRb, retinoblastoma protein; PCNA, proliferating cell nuclear antigen;TIMP, tissue inhibitor of metalloproteinase.

  • ↵1-150 Regression of previously formed lesion, as opposed to inhibition of lesion formation.