Plasminogen activator inhibitor-1 is induced in microvascular endothelial cells by a chondrocyte-derived transforming growth factor-beta

Biochem Biophys Res Commun. 1991 Apr 30;176(2):633-8. doi: 10.1016/s0006-291x(05)80231-1.


We have previously demonstrated that a chondrocyte-derived TGF-beta inhibits spontaneous endothelial sprout formation in an in vitro model of angiogenesis (Pepper et al., J.Cell.Physiol. 146:170-179, 1991). We suggested that the inhibition might be mediated by an antiproteolytic effect. In this paper, we describe the induction of PAI-1 and PAI-1 mRNA in microvascular endothelial cells by chondrocyte conditioned medium. This effect can be significantly reduced by the addition of anti-TGF-beta antibodies to the conditioned medium, and can be mimicked by the addition of exogenous TGF-beta 1. Taken together with our previous observations, these results demonstrate that the inhibition of endothelial sprout formation occurs concomitantly with an increase in the production of PAI-1, a physiological plasminogen activator inhibitor. This suggests that TGF-beta-induced antiproteolysis is responsible for the inhibition of sprout formation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies / immunology
  • Chick Embryo
  • Culture Techniques
  • Endothelium, Vascular / metabolism*
  • Plasminogen Inactivators / immunology
  • Plasminogen Inactivators / metabolism*
  • Proteins / genetics
  • Proteins / immunology
  • Proteins / metabolism*
  • RNA, Messenger / metabolism
  • Transforming Growth Factors / genetics
  • Transforming Growth Factors / immunology
  • Transforming Growth Factors / metabolism*


  • Antibodies
  • Plasminogen Inactivators
  • Proteins
  • RNA, Messenger
  • Transforming Growth Factors