Effects of Vanadate on Prostacyclin and Endothelin-1 Production and Protein-Tyrosine Phosphorylation in Human Endothelial Cells

Summary

The ability of vanadate, an inhibitor of protein-tyrosine phosphatases, to affect the production of prostacyclin (PGI2) and endothelin-1 (ET-1) and protein-tyrosine phosphorylation in human umbilical vein endothelial cells (HUVEC) was studied. The addition of vanadate to monolayers of cultured HUVEC caused a sustained release of PGI₂ from HUVEC in a time- and dose-dependent manner. When aspirin-treated HUVEC, which have lost the ability to increase PGI₂ production in response to arachidonate, were incubated with vanadate, the cells recovered their ability to increase PGI₂ production in response to arachidonate. This recovery of inducible PGI₂ production in aspirin-treated HUVEC was completely inhibited either by cycloheximide, a protein synthesis inhibitor, or by actinomycin D, an RNA synthesis inhibitor. In contrast, the same concentration of vanadate suppressed the basal release of ET-1 from HUVEC. Vanadate also caused an increase in protein-tyrosine phosphorylation in HUVEC. These data indicate that vanadate induces opposite effects on PGI₂ and ET-1 production with a concomitant increase in protein-tyrosine phosphorylation in HUVEC.

• References

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