Insulin-like growth factor-1 protects from vascular stenosis and accelerates re-endothelialization in a rat model of carotid artery injury

J Thromb Haemost. 2009 Nov;7(11):1920-8. doi: 10.1111/j.1538-7836.2009.03607.x. Epub 2009 Sep 9.


Background: IGF-1 is a potent mitogen for vascular smooth muscle cells, but exerts protective effects on endothelial cells that may trigger antiatherogenic mechanisms.

Objectives: This study was designed to test the hypothesis that an IGF-1 excess following arterial injury prevents neointima formation and vascular stenosis.

Methods: Rats were subjected to carotid balloon injury and treated with IGF-1 (1.2 mg kg(-1) per die) or saline for 10 days.

Results: In IGF-1 treated animals, high tissue levels of eNOS, Akt and its phosphorylated form were found, confirming activation of IGF-1-dependent signaling pathways. IGF-1 markedly reduced neointima formation and post-injury arterial stenosis. IGF-1 exerted proliferative and anti-apoptotic effects in the media of injured carotids, but inhibited mitotic activity and induced apoptosis in the neointima. Furthermore, IGF-1 stimulated mobilization of progenitor endothelial cells and re-endothelialization of the injured arteries. L-NAME administration inhibited IGF-1 vasculoprotective effects.

Conclusions: IGF-1 attenuates post-injury carotid stenosis by exerting differential effects in the neointima and tunica media with regard to the key components of the response to injury. The data point to a novel role of IGF-1 as a potent vasculoprotective factor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carotid Artery Injuries*
  • Carotid Stenosis*
  • Catheterization / adverse effects
  • Disease Models, Animal
  • Endothelium, Vascular / physiology*
  • Insulin-Like Growth Factor I*
  • Protective Agents
  • Rats
  • Regeneration*
  • Tunica Intima
  • Tunica Media


  • Protective Agents
  • Insulin-Like Growth Factor I