Biochemical and Biophysical Research Communications 1993-10-15

Endothelin-3 mediated proliferation in wounded human umbilical vein endothelial cells.

A D Wren, C R Hiley, T P Fan

Index: Biochem. Biophys. Res. Commun. 196(1) , 369-75, (1993)

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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.