, Volume 103, Issue 6, pp 572-581
Date: 05 Jul 2008

Impaired interaction of platelets with endothelial progenitor cells in patients with cardiovascular risk factors

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Recent studies indicate that platelets influence endothelial progenitor cell (EPC) recruitment to sites of vascular injury and promote their differentiation to an endothelial phenotype. Patients with cardiovascular risk factors (CVRF) demonstrate a reduced number and impaired function of EPC, as well as platelet hyper-reactivity. Therefore, we investigated the interaction of platelets and EPC from patients with CVRF.

Methods and results

Co-incubation of platelets and peripheral blood mononuclear cells, both from healthy volunteers, dose-dependently increased the number of adherent EPC. In contrast, patient-derived platelets failed to augment the number of adherent and migrating healthy and patient-derived EPC. However, co-incubation of platelets from healthy donors with mononuclear cells from patients with CVRF significantly enhanced the number of EPC, indicating that platelets from healthy volunteers are able to partially rescue the impairment of patient-derived EPC formation. Likewise, healthy donor-derived platelets augmented the impaired migration and clonal capacity of patient-derived EPC. Analysis of individual CVRF of platelet donors revealed that only diabetes mellitus inversely correlated with EPC number, colony formation and migration. The platelet supernatants from healthy volunteers that significantly increased EPC number contained IL-6, SDF-1, sCD40L and PDGF. While sCD40L and PDGF levels were comparable in platelet supernatants from healthy volunteers and patients with CVRF, the release of IL-6 and SDF-1 by patient-derived platelets was rather increased, thus, indicating that these soluble factors are not mediating the effect of platelet supernatants.


Healthy volunteer-derived platelets provide a source of soluble factors to improve the number and function of EPC from patients with cardiovascular risk factors, particularly diabetes mellitus.

Returned for 1. Revision: 17 October 2007 1. Revision received: 5 May 2008
Returned for 2. Revision: 4 June 2008 2. Revision received: 9 June 2008