Summary
Heparin in combination with endothelial cell growth factor (ECGF) affects physiological
responses and growth of human umbilical vein endothelial cells (HUVEC). We have examined
the effect of heparin, crude ECGF (endothelial cell growth supplement [ECGS]), or
both on the basal and thrombin challenged output of metabolites by HUVEC. The supernatant
and/or cell lysate was assayed for released prostacyclin, von Willebrand factor, tissue
plasminogen activator, plasminogen activator inhibitor and thrombospondin. Heparin
modified release of all these metabolites when in combination with ECGS, and in general
these responses were the opposite of those generated by inflammatory mediators such
as interleukin-1. It has been postulated that heparin acts by potentiating the effect
of ECGF, but heparin inhibited thrombospondin release and enhanced that of von Willebrand
factor in the absence of ECGS, while ECGS alone inhibited release of plasminogen activator
inhibitor. Thus, under our experimental conditions it would appear that heparin and
crude ECGF can affect HUVEC independently of one another.
