title: Endothelin-3 mediated proliferation in wounded human umbilical vein endothelial cells.
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.
authors.affiliation: Department of Pharmacology, University of Cambridge, England.
authors.forename: A D
authors.initials: AD
authors.lastname: Wren
authors.forename: C R
authors.initials: CR
authors.lastname: Hiley
authors.forename: T P
authors.initials: TP
authors.lastname: Fan
mesh_terms: D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D065128:Endothelin Receptor Antagonists; D016232:Endothelins / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000254:growth & development* / Q000473:pathology*; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D008954:Models, Biological; D014471:Umbilical Veins / Q000166:cytology; D014757:Viper Venoms / Q000494:pharmacology; D014945:Wound Healing / Q000502:physiology
chemical_list: D065128:Endothelin Receptor Antagonists; D016232:Endothelins; D014757:Viper Venoms; C057354:sarafotoxins s6; C061779:endothelin 1, Ala(1,3,11,15)-; D007213:Indomethacin