CD39 and endothelial cells
Endothelial cells and related vascular smooth muscle cells express CD39,
which plays a key role in inflammation and thrombus reduction[93]. CD39 expressed by vascular endothelial cells
could limit excessive polymorphonuclear leukocyte infiltration by
providing increased ADO concentrations at hypoxic and inflammation sites[60]. The arterial expression and functionality of
CD39 is decreased in hypertension. The reduced ectonucleotidase activity
of CD39 may enhance pathology-associated vascular damage, increase
endothelial permeability and inflammation, and increase the risk of
end-organ damage and thrombogenesis [94]. In tumor
environment, the expression of CD39 in vascular system, especially
endothelial cells, can promote tumor growth by scavenging eATP[95]. The endothelial CD39/CD73 axis regulates
hemostasis by transforming the local environment from a prethrombotic
state rich in ATP and ADP into an antithrombotic environment rich in ADO[96-98]. CD39 plays the role of an endothelial
thromboregulator by demonstrating that CD39-transfected COS cells
acquire the ability to inhibit ADP-induced aggregation in platelet-rich
plasma [99-101]. Next to inhibition of platelet
activation, the local release of CD39 mRNA in atherosclerotic blood
vessels supports the integrity of the endothelium and inhibits
extracellular nucleotide-induced smooth muscle cell proliferation[102]. Paradoxically, Aho et al. showed that
elevated eATP or inhibition of CD39 activity has a protective effect
against DNA damage in endothelial cells [103].
However, this effect could not be replicated in cancer cells.