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Thromb Haemost 1994; 72(06): 973-978
DOI: 10.1055/s-0038-1648992
Original Article
Schattauer GmbH Stuttgart

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

Hiromasa Shimizu
1   The First Department of Internal Medicine, Japan
,
Hiroshi Takayama
1   The First Department of Internal Medicine, Japan
,
Jong-Dae Lee
1   The First Department of Internal Medicine, Japan
,
Kazuo Satake
1   The First Department of Internal Medicine, Japan
,
Takanobu Taniguchi
2   Department of Biochemistry, Fukui Medical School, Matsuoka, Fukui, Japan
,
Hirohei Yamamura
2   Department of Biochemistry, Fukui Medical School, Matsuoka, Fukui, Japan
,
Toru Nakamura
1   The First Department of Internal Medicine, Japan
› Author Affiliations
Further Information

Publication History

Received 14 September 1993

Accepted after resubmission 12 July 1994

Publication Date:
06 July 2018 (online)

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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.

 

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