Dominant negative insulin-like growth factor-1 receptor inhibits neointimal formation through suppression of vascular smooth muscle cell migration and proliferation, and induction of apoptosis

Biochem Biophys Res Commun. 2004 Dec 17;325(3):1106-14. doi: 10.1016/j.bbrc.2004.10.175.

Abstract

Blocking of the IGF-1 signaling pathway targeting the IGF-1 receptor (IGF-1R) provides a potential treatment strategy for restenosis. In this study, we have examined the effects of a dominant negative IGF-1R (IGF-1Rt) on primary rat VSMCs in vitro and on injured rat carotid artery in vivo. Ad/IGF-1Rt infection inhibited VSMC migration and proliferation, and it also induced apoptosis by inhibiting phosphorylation of Akt and phosphorylation of ERK1/2. Consistent with the anti-proliferative and apoptotic effects in vitro, the Ad/IGF-1Rt infection markedly reduced neointimal formation in carotid injury model. Ad/IGF-1Rt treated carotid arteries exhibited a suppressed proliferation index, PCNA expression, and also were stained positive for TUNEL assay. These results indicate that a dominant negative IGF-1R has the potential to reduce neointimal formation of injured rats' carotid arteries. The delivery of dominant negative IGF-1R by adenoviral or other vectors may provide a useful strategy for inhibiting restenosis after angioplasty.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angioplasty, Balloon / adverse effects
  • Animals
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Cell Movement / drug effects
  • Cell Movement / genetics
  • Cell Proliferation / drug effects
  • Cells, Cultured
  • Coronary Restenosis / etiology
  • Coronary Restenosis / genetics
  • Coronary Restenosis / pathology*
  • Coronary Restenosis / prevention & control*
  • Gene Transfer Techniques*
  • Genes, Dominant / genetics
  • Genetic Therapy / methods
  • Male
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / physiopathology*
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, IGF Type 1 / agonists*
  • Receptor, IGF Type 1 / genetics*
  • Treatment Outcome
  • Tunica Intima / drug effects
  • Tunica Intima / growth & development
  • Tunica Intima / pathology

Substances

  • Receptor, IGF Type 1