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Effects of Dual Purinoceptor-Dependent Approach on Release of Vascular Endothelial Growth Factor from Human Microvascular Endothelial Cell (HMEC-1) and Endothelial Cell Condition.

In the recent years the awareness of the role purinergic signaling plays as a therapeutic target has increased considerably. The purinoceptor allows the action of extracellular nucleotides (P2 receptors), as well as intermediary products of their metabolism, such as adenosine (P1 receptors), regulating pivotal processes occurring in the cardiovascular system.This study focuses on a dual purinoreceptor-dependent approach, based on the activation of adenosine P1 receptors with the simultaneous inhibition of P2Y12 receptors, that can be used as novel platelet inhibitors in antithrombotic therapy.Endothelial cells are directly exposed to the drugs circulating in the bloodstream. That's why effects of our concept on human microvascular endothelial cells (HMEC-1) were examined in in vitro studies: ELISA and Scratch Assays. In response to adenosine receptor agonists, levels of secreted VEGF varied. Two of them, NECA and MRE0094 remarkably increased VEGF release. The elevated levels were reduced when used together with the P2Y12 receptor antagonist. Also, rates of wound closure in Scratch Assay were significantly reduced in these cases.The results suggest that the proposed treatment does not impair endothelial cell condition. In addition, it is suggested a collateral benefit, namely solving the problem of excessive activation of endothelial cells during antiplatelet therapy.