Key result
Vanadate induced the expression of COX-1 and COX-2 mRNAs in human umbilical vein endothelial cells, an effect that was inhibited by the protein-tyrosine kinase inhibitor Tyrphostin-47.
Activation of protein-tyrosine kinases is causally linked to the expression of COX-1 and COX-2 mRNAs in human endothelial cells.
Tyrosine kinase signaling may regulate endothelial COX expression; leaves open relevance to vascular inflammation in vivo.
Endothelial cells possess constitutive or inducible cyclo-oxygenase (COX) isoenzymes for prostacyclin production, but the mechanisms for their expression are largely unknown. We found that vanadate, an inhibitor of protein-tyrosine phosphatases, induced the expression of two COX isoenzyme mRNAs in human umbilical vein endothelial cells (HUVEC) in a time- and dose-dependent manner. Vanadate also stimulated an increase in COX-2 protein levels, but did not affect significantly the levels of constitutively expressed COX-1 protein. Synergistic enhancement of expression of the two COX isoenzyme mRNAs was observed on stimulation of HUVEC with vanadate plus interleukin-1alpha. Tyrphostin-47, which as an inhibitor of protein-tyrosine kinases abolished vanadate-induced protein-tyrosine phosphorylation, inhibited expression of the two COX isoenzyme mRNAs in HUVEC stimulated with vanadate or interleukin-1alpha. These data provide conclusive evidence that activation of protein-tyrosine kinases is causally linked to expression of the mRNAs for the two COX isoenzymes in HUVEC.
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Hirai et al. (1997) studied this question. Vanadate and Tyrphostin-47 was evaluated on Expression of COX-1 and COX-2 mRNAs and proteins. Vanadate induced the expression of COX-1 and COX-2 mRNAs in human umbilical vein endothelial cells, an effect that was inhibited by the protein-tyrosine kinase inhibitor Tyrphostin-47.
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