Endothelin-3 Mediated Proliferation in Wounded Human Umbilical Vein Endothelial Cells

Biochem Biophys Res Commun. 1993 Oct 15;196(1):369-75. doi: 10.1006/bbrc.1993.2258.

Abstract

An in vitro model of endothelial cell injury was used to investigate the role of endothelins and related peptides in endothelial repair. Endothelin-3 (10-100 nM) enhanced wound repair over an 18 h period by promoting proliferation, an effect not inhibited by the specific ETA receptor antagonist BQ-123 (100 nM) or the mixed ETA/ETB antagonist PD142893 (10 microM). Like endothelin-3, the ETB selective agonists [Ala1,3,11,15]endothelin-1 and sarafotoxin S6c were able to enhance wound repair over the same dose range. Neither endothelin-1 nor endothelin-2, however, had any effect on endothelial cell wound healing. Inhibition of cyclo-oxygenase or neutralisation of basic fibroblast growth factor did not inhibit this endothelin-3-mediated event. These results suggest that endothelin-3 might have a direct role in endothelial cell proliferation as a response to injury which is not mediated by either of the currently defined ETA and ETB receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Division / drug effects
  • Cells, Cultured
  • Endothelin Receptor Antagonists
  • Endothelins / pharmacology*
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / growth & development*
  • Endothelium, Vascular / pathology*
  • Humans
  • Indomethacin / pharmacology
  • Models, Biological
  • Umbilical Veins / cytology
  • Viper Venoms / pharmacology
  • Wound Healing / physiology

Substances

  • Endothelin Receptor Antagonists
  • Endothelins
  • Viper Venoms
  • sarafotoxins s6
  • endothelin 1, Ala(1,3,11,15)-
  • Indomethacin