Thromb Haemost 2006; 96(04): 498-504
DOI: 10.1160/TH06-05-0250
Platelets and Blood Cells
Schattauer GmbH

Potential role of activated platelets in homing of human endothelial progenitor cells to subendothelial matrix

Eli I. Lev
1   The Methodist Hospital Research Institute and The Methodist DeBakey Heart Center, Houston, Texas, USA
,
Zeev Estrov
2   The Methodist Hospital, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
,
Khatira Aboulfatova
3   Thrombosis Research Section, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
,
David Harris
2   The Methodist Hospital, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
,
Juan F. Granada
1   The Methodist Hospital Research Institute and The Methodist DeBakey Heart Center, Houston, Texas, USA
,
Carlos Alviar
1   The Methodist Hospital Research Institute and The Methodist DeBakey Heart Center, Houston, Texas, USA
,
Neal S. Kleiman
1   The Methodist Hospital Research Institute and The Methodist DeBakey Heart Center, Houston, Texas, USA
,
Jing-fei Dong
3   Thrombosis Research Section, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
› Author Affiliations
Further Information

Publication History

Received 08 May 2006

Accepted after resubmission 31 July 2006

Publication Date:
29 November 2017 (online)

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Summary

Endothelial progenitor cells (EPCs) mobilize from the bone marrow in response to tissue injury and participate in vascular repair. However, there is limited data about the homing mechanisms of EPCs to vascular injury sites. Recently animal experiments indicated that platelets playa role in recruitment of EPCs to injury sites. However, data on the possible interaction between platelets and EPCs within the human system are limited. We, therefore, examined in-vitro human platelet-EPC interaction under static and flow conditions. Human EPCs were isolated from donated buffy coats by magnetic microbeads and flow cytometry cell sorting using CD133 and VEGFR-2, respectively, as markers. Platelets were tested in the form of washed platelets, platelet rich plasma or whole blood. EPCs formed heterotypic aggregates with resting platelets under static conditions, an interaction that was greatly enhanced when platelets were activated by collagen, ADP or thrombin-activation peptide. The platelet-EPC interaction was inhibited by antibodies to P-selectin or P-selectin glycoprotein ligand-1 (PSGL-1), but not by antibodies to glycoproteins Ib-IX-V or IIb/IIIa. When perfused over activated platelets under shear stress of 2.5 dyn/cm2, EPCs tethered to platelayers and either adhered immediately or rolled a short distance before adhering. In addition, platelets promoted the colonization of adherent EPCs in culture conditions. Consistent with recent animal studies, these findings demonstrate that human EPCs interact in vitro with activated platelets under static and flow conditions, mediated through P-selectin–PSGL-1 interaction. This interaction may be a central mechanism for homing of EPCs to vascular injury sites.