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  • American Society of Hematology  (4)
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  • American Society of Hematology  (4)
Sprache
Erscheinungszeitraum
Fachgebiete(RVK)
  • 1
    In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 3938-3938
    Kurzfassung: We and others have found that platelets play an important role in the recruitment of endothelial progenitor cells to sights of vascular injury. However, it is not clear whether the EPCs mature and differentiate to endothelial cells following recruitment to the vascular injury sites. In addition, there is limited in vivo data to support the role of EPCs in re-endothlialization following vascular injury. We conducted in vitro experiments to investigate the maturation of EPCs on platelet based-media and in vivo experiments to evaluate the recruitment of EPCs following vascular injury. In in vitro experiments human EPCs were isolated from donated buffy coats by magnetic microbeads and flow cytometry cell sorting using CD133 and VEGFR-2, respectively, as cell markers. Isolated viable EPCs (CD133+, VEGFR-2+ cells) were plated on human fibronectin or a monolayer of washed human platelets. Cell colonies were counted 7 days after plating and stained for the endothelial cell markers CD31 (PECAM-1) and CD144 (VE-cadherin). The mean number of colony-forming cells was 35±2.6 colonies/106 cells on platelets, which was significantly higher than 18±4.2 colonies/106 cells on fibronectin (n = 4, P & lt;0.01). Apart from the difference in colony numbers, the EPC colonies grew faster on the platelet substrate, were larger, and had more spindle-shaped cells (Figure 1 - staining of EPC colonies for CD31 and CD144). In the in vivo experiments a model of transluminal injury to mouse femoral arteries was used. Femoral artery denudation was performed by 0.25-mm-diameter angioplasty guidewire. Injured femoral arteries were compared to the contra-lateral controls (uninjured), and were harvested 1.5 hours following the injury and immunostaining performed with an anti-VEGFR-2 antibody. Four experiments showed a markedly higher number of VEGFR-2+ cells in the artery that has undergone denudation. These experiments indicate that a media composed of platelets promotes the maturation and differentiation of EPCs. Furthermore, in vivo, EPCs are recruited early following vascular injury. Thus, homing, maturation, and differentiation of EPCs are mediated by platelets.
    Materialart: Online-Ressource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Society of Hematology
    Publikationsdatum: 2006
    ZDB Id: 1468538-3
    ZDB Id: 80069-7
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 2
    In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 3682-3682
    Kurzfassung: Endothelial progenitor cells (EPCs) are bone marrow-derived undifferentiated cells that are rapidly mobilized in response to tissue ischemia and incorporated into sites of neovascularization. EPCs co-express surface CD34, CD133 and vascular endothelial growth factor receptor-2 (VEGFR-2) antigens and develop an endothelial phenotype in culture. In animal models of tissue ischemia EPCs were shown to participate in angiogenesis and vasculogenesis. We sought to determine whether circulating EPCs level correlate with collateral formation following a non-ST segment elevation myocardial infarction (NSTEMI). In addition, we sought to evaluate the effect of percutaneous coronary intervention (PCI) on the levels of circulating EPCs. Twenty patients who underwent PCI within a week of NSTEMI were divided into two groups: patients without collaterals [coll(−), n=10] and patients with Rentrop grade 3–4 collaterals [coll(+), n=10] . Two blood samples were drawn from all patients: before PCI and 24±2 hours after PCI. Using flow cytometry the percentage of cells co-expressing VEGFR-2 and CD133 was determined. In addition, EPC colonies were grown from peripheral blood mononuclear cells, characterized, and counted after 7 days of culture. The clinical characteristics of the two groups were similar. The coll(+) group had a higher degree of culprit vessel stenosis and lower initial TIMI flow grade. The relative number of EPCs (co-expressing VEGFR-2 and CD133) before PCI was significantly higher in the coll(+) group than in the coll(−) group (1.49±0.9% vs. 0.77±0.4%, P=0.045). There were no significant inter-group differences in the number of EPC colony-forming cells. The number of EPC colonies increased significantly in the coll(−) group following PCI (from 9.5±4.8 to 14.0±5.9 per 106 cultured cells, P=0.01). This study supports an association between circulating EPC levels and collateral formation in patients with a NSTEMI. Furthermore, these findings suggest that vascular injury during PCI triggers mobilization of EPCs to the peripheral blood, especially in patients without coronary collaterals. Our data suggest that patients with high levels of circulating EPCs are more likely to form coronary artery collaterals and that vascular injury induces EPC recruitment.
    Materialart: Online-Ressource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Society of Hematology
    Publikationsdatum: 2005
    ZDB Id: 1468538-3
    ZDB Id: 80069-7
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 3
    Online-Ressource
    Online-Ressource
    American Society of Hematology ; 2016
    In:  Blood Vol. 127, No. 23 ( 2016-06-09), p. 2788-2789
    In: Blood, American Society of Hematology, Vol. 127, No. 23 ( 2016-06-09), p. 2788-2789
    Materialart: Online-Ressource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Society of Hematology
    Publikationsdatum: 2016
    ZDB Id: 1468538-3
    ZDB Id: 80069-7
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 4
    Online-Ressource
    Online-Ressource
    American Society of Hematology ; 2005
    In:  Blood Vol. 106, No. 11 ( 2005-11-16), p. 3681-3681
    In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 3681-3681
    Kurzfassung: Endothelial Progenitor Cells (EPCs) are undifferentiated bone marrow cells that are rapidly mobilized upon vascular or tissue injury. The circulating EPCs home to and differentiate at the site of vessel injury to enhance repair of damaged endothelium. Much has been learnt of how EPCs adhere to and transmigrate on endothelial cells during angiogenesis, but little is know about how EPCs home to the site where endothelial cells are denuded and subendothelium is exposed following vascular injury. We hypothesized that platelets mediate EPC homing because they are the first cells that tether and adhere to subendothelium exposed by vascular injury. To test this hypothesis, we examined the platelet-EPC interaction under static and flow conditions. Human EPCs were purified from buffy coats by cell sorting using CD133 and VEGFR-2 as the cell markers. The EPCs were then incubated with washed platelets that were either at resting state or activated by 5 mg/ml of collagen. EPC-platelet interaction was measured in the form of heterotypic aggregation between two types of cells by flow cytometry (dual labeled with FITC-CD42a and PE-CD133). We found the EPCs attached to resting platelets, however, the percentage of platelets binding to EPCs significantly increased when platelets were activated by collagen (1.02% vs. 2.76%, p & lt; 0.05). EPC-platelet aggregation was similarly detected in whole blood and platelet-rich plasma. When perfused over a monolayer of activated platelets under a shear stress of 2.5 dyn/cm2, the CD133 positive EPCs tethered to the platelet monolayer. The tethered EPCs either firmly adhered immediately or rolled a short distance before becoming adherent. This EPC-platelet interaction was calcium-dependent and inhibited by up to 60±11.5% by a polyclonal P-selectin antibody. In comparison, the monoclonal GP Iba antibody AK2, which blocks GP Ib-VWF interaction, had no effect. These results demonstrate for the first time a significant interaction between EPCs and activated platelets both at static and flow conditions. Our findings suggest that platelets may function as carrier cells that direct EPCs to the site of vascular injury. In addition to homing, platelets, which release several growth factors known to affect EPCs, may provide a supporting matrix on which adherent EPCs proliferate and differentiate.
    Materialart: Online-Ressource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Society of Hematology
    Publikationsdatum: 2005
    ZDB Id: 1468538-3
    ZDB Id: 80069-7
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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