Basic study for development of a novel therapeutic strategy, targeting the extracellular ATP hydrolyzing enzyme, CD39 to protect from vascular endothelial disorder.

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Vascular endothelial cells express highly active ecto-nucleoside diphosphohydrolase 1 (CD39) that hydrolyzes extracellular ATP and ADP into AMP. CD39 plays a critical role in the regulation of vascular homeostasis. In this study, we found that various inflammatory cytokines including IL-1β, TNF-α and IFN-γ, impaired the ATP hydrolysis and CD39 mRNA expression, whereas HMG-CoA reductase inhibitor (statin) caused time- and concentration-dependent increase in ATP and ADP hydrolysis accompanied by an up-regulation of CD39 mRNA expression. Statin-induced up-regulation of CD39 mRNA expression was involved in an inhibition of small G protein Rho function. These results suggest that the inhibition of Rho-dependent signaling is a promising strategy to increases vascular CD39 expression.