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  • Ovid Technologies (Wolters Kluwer Health)  (7)
  • Cho, Hyun-Jai  (7)
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  • Ovid Technologies (Wolters Kluwer Health)  (7)
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  • 1
    Online Resource
    Online Resource
    Abstract P120: Improving the Angiogenic Abilities of Mobilized Peripheral Blood Stem Cells Achieved by Priming with Activated Platelet Supernatant for Regenerative Cell Therapy
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Hypertension Vol. 66, No. suppl_1 ( 2015-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 66, No. suppl_1 ( 2015-09)
    Abstract: Platelets play a critical role in hemostasis and also have ability to promote angiogenesis and tissue repair by secreting of numerous cytokine and making angiogenic condition. We investigated whether autologous ‘activated platelet supernatant (APS)’ has effect on enhancing pro-angiogenic potential of peripheral blood stem cells (PBSC) for stem cell-based therapy for ischemic diseases. Granulocyte-colony stimulating factor (G-CSF) mobilized peripheral blood stem cells (mobPBSC) were isolated from healthy volunteers, while APS was collected from platelet rich plasma by thrombin activation. mobPBSCs were primed with APS (APS primed mobPBSCs) for 6 hours, and APS primed mobPBSCs characterized their angiogenic ability. For the safety analysis, we estimated the thrombogenicity of platelets in whole blood mixed with APS primed mobPBSCs by expression of glycoprotein IIb and IIIa on platelets. APS had a higher level of various cytokines, such as IL8, IL17, PDGF and VEGF than naïve platelet supernatants. And APS primed mobPBSCs had more expression of angiogenic factors, surface markers (i.e. CD34, CD31, and CXCR4) and integrins (integrin α5, β1 and β2) than Veh primed and Pre primed mobPBSC. Also APS primed mobPBSCs were polarized toward CD14++/CD16+ pro-angiogenic monocytes. And result in adhesion to endothelial cells and fibronectin which represents cell to cell and cell to extracellular matrix adhesion, respectively. The culture supernatant of APS-primed mobPBSCs contained high levels of IL8, IL10, IL17 and TNFα, and augmented proliferation and capillary network formation of HUVEC. In-vivo transplantation of APS-primed mobPBSC into athymic mice ischemic hindlimbs and Matrigel plugs elicited vessel differentiation and tissue repair. In thrombogenicity test, platelet activity increased after mixing whole blood with mobPBSC regardless of the priming agent. However, this was reduced by pretreatment of aspirin, which is an antiplatelet agent prescribed to patients with ischemic diseases. Our data demonstrate that mobPBSCs primed with APS improve angiogenic potential, and that can be adjunctive strategy to enhance the efficiency of stem cell therapy for ischemic diseases.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.66.suppl_1.p120
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2094210-2
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  • 2
    Online Resource
    Online Resource
    New Mechanism of Rosiglitazone to Reduce Neointimal Hyperplasia : Activation of Glycogen Synthase Kinase-3β Followed by Inhibition of MMP-9
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 29, No. 4 ( 2009-04), p. 472-479
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 29, No. 4 ( 2009-04), p. 472-479
    Abstract: Rosiglitazone regulated both VSMC viability and migration through activation of GSK-3β, resulting in reduced neointimal hyperplasia after vascular injury. The mechanism to inhibit migration was that rosiglitazone suppressed MMP-9 via GSK-3β mediated inhibition of NF-κB DNA binding activity. Our results demonstrate new action mechanism of rosiglitazone to reduce neointimal hyperplasia and may provide rosiglitazone as a new therapeutic approach for proliferative vascular disease.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.108.176230
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 1494427-3
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  • 3
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    Online Resource
    Enhanced Clopidogrel Responsiveness in Smokers : Smokers' Paradox Is Dependent on Cytochrome P450 CYP1A2 Status
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 31, No. 3 ( 2011-03), p. 665-671
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 3 ( 2011-03), p. 665-671
    Abstract: Observational studies have reported enhanced response to clopidogrel in smokers (the smokers' paradox). We examined whether genetic variations in the cytochrome and drug transporter system are associated with the effect of smoking on clopidogrel response. Methods and Results— Clopidogrel on-treatment platelet reactivity (OPR) was measured in 1431 consecutive patients who underwent coronary angiography. Gene samples were available and genotyping was successful in 1123 patients. Nine candidate single-nucleotide polymorphisms in 5 cytochrome genes and 1 drug transporter gene were assessed. The mean OPR of the entire population was 241.9±79.3 (P2Y 12 reaction units). Two hundred forty-nine (17%) smokers had lower OPR compared with 1182 (83%) nonsmokers (227.6±76.0 versus 244.9±79.7, P =0.001). Among the 9 single-nucleotide polymorphisms, only CYP1A2 showed a genotype-dependent change in the effect of smoking on OPR. After adjustment for possible confounding factors, cigarette smoking was associated with a lower OPR by −19 P2Y 12 reaction units ( P =0.009) and lower risk for high OPR (odds ratio [OR], 0.48; 95% CI, 0.31 to 0.74) in the AA and CA genotypes but not in the CC genotype. Conclusion— Enhanced clopidogrel response in smokers, known as the smokers' paradox, is not universal but was observed only in cytochrome P450 CYP1A2 (−163C 〉 A) A-allele carriers, suggesting a genotype-dependent effect of smoking on clopidogrel responsiveness.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.110.217182
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 1494427-3
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  • 4
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    Online Resource
    Peroxisome Proliferator–Activated Receptor-δ Agonist Enhances Vasculogenesis by Regulating Endothelial Progenitor Cells Through Genomic and Nongenomic Activations of the Phosphatidylinositol 3-Kinase/Akt Pathway
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. 10 ( 2008-09-02), p. 1021-1033
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. 10 ( 2008-09-02), p. 1021-1033
    Abstract: Background— Despite the therapeutic potential of endothelial progenitor cells (EPCs) in ischemic vascular diseases, their insufficient numbers limit clinical applications. Peroxisome proliferator–activated receptor (PPAR)-δ belongs to the nuclear hormone receptor superfamily, and its functions in various tissues and cells are almost unexplored, especially with respect to vascular biology. Methods and Results— PPAR-δ activation in EPCs phosphorylated Akt, and this phosphorylation was mediated not only by genomic but also by nongenomic pathways through interaction with the regulatory subunit of phosphatidylinositol 3-kinase. PPAR-δ activation with agonist (GW501516 or L-165041) increased the proliferation of human EPCs and protected them from hypoxia-induced apoptosis. In addition, PPAR-δ activation enhanced EPC functions, such as transendothelial migration, and tube formation. These actions by PPAR-δ activation in EPCs were dependent on the phosphatidylinositol 3-kinase/Akt pathway. In ischemic hindlimb of mice models, transplantation of PPAR-δ agonist–treated human or mouse EPCs enhanced blood flow recovery to ischemic limbs compared with vehicle-treated EPCs. In EPCs from PPAR-δ–knockout mice, however, treatment with PPAR-δ agonist did not enhance in vivo vasculogenic potential. Systemic administration of PPAR-δ agonist increased hematopoietic stem cells in bone marrow and EPCs in peripheral blood, leading to improved vasculogenesis with incorporation of bone marrow–derived cells to new vessels in a corneal neovascularization model and limb salvage with better blood flow in an ischemic hindlimb model. Conclusions— The results of our study suggest that PPAR-δ agonist has therapeutic vasculogenic potential for the treatment of ischemic cardiovascular diseases.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.108.777169
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1466401-X
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  • 5
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    Online Resource
    Abstract P119: Human Podoplanin+/vegfr-3+/lyve-1+ Monocytes are Lymphatic Endothelial Precursors
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Hypertension Vol. 66, No. suppl_1 ( 2015-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 66, No. suppl_1 ( 2015-09)
    Abstract: Lymphatic vessels are involved in the development of various inflammatory disorders, and lymphatic vessel regeneration has been increasingly investigated to develop therapies for lymphatic diseases. Here we report that Podoplanin+/VEGFR-3+/LYVE-1+ is a valid marker for human lymphatic endothelial precursors and the triple-positive cells can be used in lymphatic regeneration. During 5-day culture on an ultra-low attachment surface dish, human peripheral blood mononuclear cells (PBMCs) underwent exponential growth, aggregating into a sphere-like structure and expressing several lymphatic endothelial cell (LEC) markers and lymphangiogenic transcription factors. When dissociated from the aggregate and cultured on a gelatin-coated dish, the cells were attached to the surface. The attached cells were triple positive for LEC markers e.g. Podoplanin, LYVE-1, VEGFR-3. Furthermore, seeded in Matrigel with LECs, the 5-day aggregate-derived cells were incorporated into lymphatic endothelial network. The 5-day aggregates were largely positive for CD14+, a monocyte marker. The CD14+ population was sorted into Podoplanin-positive and negative group for further characterization. Notably, CD14+/Podoplanin+ cells showed increased expression of lymphangiogenic molecules (e.g. VEGFR-3, LYVE-1) both at the genetic and protein levels. Also, CD14+/Podoplanin+ cells secreted higher levels of lymphangiogenic cytokines (VEGF, HGF, PDGF-BB). ELISA results showed that CD14+/Podoplanin+ cells produced more lymphangiogenic cytokines than CD14+/Podoplanin- cells. Local injection of monocyte aggregates significantly increased lymphatic neovascularization and facilitated healing of the skin wound model of nude mice, with CD14+/Podoplanin+ group showing the most dramatic result. Our data suggests that Podoplanin-positive monocytes can be transdifferentiated into lymphatic endothelial precursor cells, and cells with triple positivity for Podoplanin, VEGFR-3, and LYVE-1 can be a promising cell source for therapy against human lymphatic vessel diseases.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.66.suppl_1.p119
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2094210-2
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  • 6
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    Online Resource
    Abstract 17581: Evidence for Circulating Stem Cells Derived from the Human Heart and Their Therapeutic Potential
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: Introduction and Hypothesis: Many studies have shown resident cardiac stem cells in myocardium as well as epicardial progenitor cells in epicardium. However, the presence of stem cells in the endocardium has not been elucidated. In this study, we identified circulating multipotent stem cells from human peripheral blood. Furthermore, we investigated the origin and the therapeutic potential of these cells. Methods and Results: We identified a new population of cells from human peripheral blood mononuclear cells, which were quite different from previously reported stem cells. Newly identified cells expressed genes such as Oct3/4, KLF4, Nanog, and c-Myc. Moreover, FACS analysis precluded the possibility that these cells might be hematopoietic stem cells. To investigate the origin of these cells, we collected peripheral blood from patients undergoing bone marrow, liver, heart, or kidney transplantation. After culturing these cells, we could confirm that these stem cells were derived from the human heart by identifying the HLA types or the STR (short tandem repeat) profiles. In addition, we demonstrated that Nuclear Factor of Activated T-cells (NFAT)-positive and CD31-positive circulating cells in peripheral blood were derived from NFAT-positive cells in the endocardium. These cells had multipotency, indicating the ability of differentiation not only into mesodermal lineages, but also into ectodermal or endodermal lineages. When injected into the mouse heart in vivo , these stem cells were differentiated into multiple lineages, resulting in the improvement of the heart function. We established more than 200 cell lines from peripheral blood of patients with coronary artery diseases, cardiomyopathies, hematologic diseases, liver diseases, and kidney diseases. Conclusions: We demonstrated the existence of novel circulating multipotent stem cells in human peripheral blood, which express NFAT. Interestingly, these cells are derived from the tissue-resident stem cells of the endocardium of the human heart. Our findings suggest that these stem cells obtainable from peripheral blood could be a promising tool for heart regeneration.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.17581
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 7
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    Online Resource
    Stent Coated With Antibody Against Vascular Endothelial-Cadherin Captures Endothelial Progenitor Cells, Accelerates Re-Endothelialization, and Reduces Neointimal Formation
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 31, No. 12 ( 2011-12), p. 2798-2805
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 12 ( 2011-12), p. 2798-2805
    Abstract: In contrast to CD34, vascular endothelial-cadherin (VE-cadherin) is exclusively expressed on the late endothelial progenitor cells (EPC) whereas not on the early or myeloid EPC. Thus, VE-cadherin could be an ideal target surface molecule to capture circulating late EPC. In the present study, we evaluated whether anti-VE–cadherin antibody-coated stents (VE-cad stents) might accelerate endothelial recovery and reduce neointimal formation through the ability of capturing EPC. Methods and Results— The stainless steel stents were coated with rabbit polyclonal anti-human VE-cadherin antibodies and exposed to EPC for 30 minutes in vitro. The number of EPC that adhered to the surface of VE-cad stents was significantly higher than bare metal stents (BMS) in vitro, which was obliterated by pretreatment of VE-cad stent with soluble VE-cadherin proteins. We deployed VE-cad stents and BMS in the rabbit right and left iliac arteries, respectively. At 48 hours after stent deployment in vivo, CD-31–positive endothelial cells adhered to VE-cad stent significantly more than to BMS. At 3 days, scanning electron microscopy showed that over 90% surface of VE-cad stents was covered with endothelial cells, which was significantly different from BMS. At 42 days, neointimal area that was filled with smooth muscle cells positive for actin or calponin was significantly smaller in VE-cad stents than in BMS by histological analysis (0.95±0.22 versus 1.34±0.43 mm 2 , respectively, P =0.02). Immuno-histochemical analysis revealed that infiltration of inflammatory cells was not significantly different between 2 stents. Conclusion— VE-cad stents captured EPC successfully in vitro, accelerated endothelial recovery on stent, and eventually reduced neointimal formation in vivo.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.111.226134
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 1494427-3
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