We have previously shown that Endothelial Progenitor Cells (EPCs) bind and inhibit platelet function and impair thrombus formation, but the surrounding mechanisms that regulate this process have not been fully described. Herein, we addressed the mechanistic action of EPCs on platelet-thrombus formation and we highlighted the role of platelet P-selectin in this process.

EPCs were generated from human peripheral blood mononuclear cells after 10 days of culture on fibronectin in conditioned media. The impact of EPCs on platelet aggregation and thrombus formation was investigated in P-selectin deficient (P-sel-/-) and their wild-type counterpart (WT) mice. EPCs significantly impaired, in a concentration dependent-manner, collagen-induced whole blood platelet aggregation in WT mice; whereas in P-sel-/- mice, EPCs had no significant effect. Moreover, in ferric chloride-injured arterial thrombosis model, infusion of EPCs significantly reduced thrombus formation in WT, but not in P-sel-/- mice. Furthermore, the number of EPCs recruited within the thrombi and along the arterial wall was reduced in P-sel-/- mice as compared to WT mice, and the relative mass of thrombi generated in EPC-treated P-sel-/- mice was significantly larger than that in EPC-treated WT mice.

EPCs impair platelet aggregation and reduce thrombus formation by a cellular mechanism implying binding to platelet P-selectin. These findings add new insights into the role of EPCs in the regulation of platelet function and thrombotic reaction during vascular repair.


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  • Received: 05 March 2012
  • Accepted: 28 March 2012
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