Antibodies against transforming growth factor-beta 1 suppress intimal hyperplasia in a rat model

J Clin Invest. 1994 Mar;93(3):1172-8. doi: 10.1172/JCI117070.


Intimal hyperplasia is induced by therapeutic vascular interventions and often results in clinically important narrowing of the vascular lumen. Examination of the role of TGF-beta 1 in a rat carotid artery injury model confirmed the presence of a previously reported increase in TGF-beta 1 mRNA in the media of injured arteries. Administration of neutralizing anti- TGF-beta 1 antibodies significantly (P < 0.05) reduced the size of the intimal lesions that developed after carotid balloon injury. A control antibody had no effect. The intimal/medial area ratio was also reduced in the anti-TGF-beta 1 group relative to controls (P < 0.01). Immunohistochemical staining showed that two TGF-beta 1-induced extracellular matrix components, EDA + fibronectin and versican, were greatly increased in the untreated neointimal lesions, but were almost completely absent from the lesions of the anti-TGF-beta 1-treated animals. We conclude that TGF-beta 1 is causally involved in the development of intimal hyperplasia, and that anti-TGF-beta 1 agents may be useful in achieving at least partial control of this condition.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies / immunology*
  • Base Sequence
  • Cell Division
  • Extracellular Matrix / metabolism
  • Hyperplasia
  • Male
  • Molecular Sequence Data
  • Muscle, Smooth, Vascular / pathology*
  • Rats
  • Rats, Sprague-Dawley
  • Transforming Growth Factor beta / immunology
  • Transforming Growth Factor beta / physiology*


  • Antibodies
  • Transforming Growth Factor beta