Nuclear factor-kappaB activity and arterial response to balloon injury

Atherosclerosis. 1997 May;131(1):59-66. doi: 10.1016/s0021-9150(96)06767-6.

Abstract

We studied the effect of arterial balloon injury on nuclear factor-kappaB (NF-kappaB) mobilization and ICAM-1 expression in untreated rats and rats treated with aspirin. Baseline NF-kappaB nuclear binding in smooth muscle cells (SMC) increased two-fold within 6 h after balloon injury. The binding returned to baseline 3 days after injury. Consistently nuclear staining of p65 active subunit increased in the medial SMC following balloon injury. There was no baseline ICAM-1 expression. Within 3 days after balloon injury there was marked medial ICAM-1 expression, that localized to neointima 7 days after injury and to regrowing endothelial cells 14 days after injury. Treatment with aspirin inhibited NF-kappaB nuclear translocation and binding and was associated with reduction of ICAM-1 expression, SMC proliferation and neointimal thickening following balloon injury. These data suggest that transient mobilization of NF-kappaB in vascular SMC after balloon injury mediates ICAM-1 expression and is involved in arterial response to balloon injury.

MeSH terms

  • Animals
  • Arteries / injuries*
  • Aspirin / pharmacology
  • Catheterization / adverse effects*
  • Cell Division
  • Cell Nucleus / metabolism
  • Endothelium, Vascular / metabolism
  • Immunohistochemistry
  • Intercellular Adhesion Molecule-1 / analysis
  • Intercellular Adhesion Molecule-1 / metabolism
  • Male
  • Muscle, Smooth, Vascular / metabolism
  • Muscle, Smooth, Vascular / ultrastructure
  • NF-kappa B / metabolism*
  • Rats
  • Rats, Sprague-Dawley

Substances

  • NF-kappa B
  • Intercellular Adhesion Molecule-1
  • Aspirin