TY - JOUR
T1 - Potential role of activated platelets in homing of human endothelial progenitor cells to subendothelial matrix
AU - Lev, Eli I.
AU - Estrov, Zeev
AU - Aboulfatova, Khatira
AU - Harris, David
AU - Granada, Juan F.
AU - Alviar, Carlos
AU - Kleiman, Neal S.
AU - Dong, Jing Fei
PY - 2006/10/1
Y1 - 2006/10/1
N2 - 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 play a 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 CDI33 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,AIDP or thrombin-activation peptide.The platelet-EPC interaction was inhibited by antibodies to P-selectin or P-selectin glycoprotein ligand-I (PSGL-I), 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-I interaction. This interaction may be a central mechanism for homing of EPCs to vascular injury sites.
AB - 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 play a 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 CDI33 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,AIDP or thrombin-activation peptide.The platelet-EPC interaction was inhibited by antibodies to P-selectin or P-selectin glycoprotein ligand-I (PSGL-I), 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-I interaction. This interaction may be a central mechanism for homing of EPCs to vascular injury sites.
KW - Endothelial progenitor cells
KW - Interaction
KW - Platelets
UR - http://www.scopus.com/inward/record.url?scp=33749834611&partnerID=8YFLogxK
U2 - 10.1160/TH06-05-0250
DO - 10.1160/TH06-05-0250
M3 - Article
AN - SCOPUS:33749834611
SN - 0340-6245
VL - 96
SP - 498
EP - 504
JO - Thrombosis and Haemostasis
JF - Thrombosis and Haemostasis
IS - 4
ER -