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stromal cell-derived factor-1alpha month download article/chapter stromal-derived factor-1 promotes rheinisch-westfälisch technische hochschule murine chemokine cxcl2/kc normal stem cells mitogen-activated protein kinase endothelial progenitor cell johann wolfgang goethe-university endothelial progenitor cells apolipoprotein e-deficient mice hypoxia-induced endothelial secretion article basic research /chemokine receptor axis full article pdf smooth muscle cell epc-derived proangiogenic mif stem cells 23 progenitor cell trafficking related subjects eepc cell clone privacy choices/manage cookies atherogenic cell recruitment murine embryonic epcs derived angiogenic factors cxc chemokine receptors promotes fibroblast migration thymosin beta4 march kl enhanced tube formation essential paracrine factor umbilical cord blood molecular cell biology progenitor cells key angiogenic chemokines endothelial cells molecular cardiovascular research apoe-deficient mice induced differentiation inhibited smc differentiation chemokine receptor 2018 endothelial differentiation european economic area van der zee scratch-wounded monolayers gerber hp genetically selected cardiomyocytes enhances plaque formation impaired b-lymphopoiesis mechanosensitive transcriptional mechanism

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• Carmeliet P (2000) VEGF gene therapy: stimulating angiogenesis or angioma-genesis?

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         headline:Differential roles of angiogenic chemokines in endothelial progenitor cell-induced angiogenesis
         description:This study aimed to analyze the role of endothelial progenitor cell (EPC)-derived angiogenic factors and chemokines in the multistep process driving angiogenesis with a focus on the recently discovered macrophage migration inhibitory factor (MIF)/chemokine receptor axis. Primary murine and murine embryonic EPCs (eEPCs) were analyzed for the expression of angiogenic/chemokines and components of the MIF/CXC chemokine receptor axis, focusing on the influence of hypoxic versus normoxic stimulation. Hypoxia induced an upregulation of CXCR2 and CXCR4 but not CD74 on EPCs and triggered the secretion of CXCL12, CXCL1, MIF, and vascular endothelial growth factor (VEGF). These factors stimulated the transmigration activity and adhesive capacity of EPCs, with MIF and VEGF exhibiting the strongest effects under hypoxia. MIF-, VEGF-, CXCL12-, and CXCL1-stimulated EPCs enhanced tube formation, with MIF and VEGF exhibiting again the strongest effect following hypoxia. Tube formation following in vivo implantation utilizing angiogenic factor-loaded Matrigel plugs was only promoted by VEGF. Coloading of plugs with eEPCs led to enhanced tube formation only by CXCL12, whereas MIF was the only factor which induced differentiation towards an endothelial and smooth muscle cell (SMC) phenotype, indicating an angiogenic and differentiation capacity in vivo. Surprisingly, CXCL12, a chemoattractant for smooth muscle progenitor cells, inhibited SMC differentiation. We have identified a role for EPC-derived proangiogenic MIF, VEGF and MIF receptors in EPC recruitment following hypoxia, EPC differentiation and subsequent tube and vessel formation, whereas CXCL12, a mediator of early EPC recruitment, does not contribute to the remodeling process. By discerning the contributions of key angiogenic chemokines and EPCs, these findings offer valuable mechanistic insight into mouse models of angiogenesis and help to define the intricate interplay between EPC-derived angiogenic cargo factors, EPCs, and the angiogenic target tissue.
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            Angiogenesis
            Hypoxia
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            Chemokine
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            Cardiology
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      headline:Differential roles of angiogenic chemokines in endothelial progenitor cell-induced angiogenesis
      description:This study aimed to analyze the role of endothelial progenitor cell (EPC)-derived angiogenic factors and chemokines in the multistep process driving angiogenesis with a focus on the recently discovered macrophage migration inhibitory factor (MIF)/chemokine receptor axis. Primary murine and murine embryonic EPCs (eEPCs) were analyzed for the expression of angiogenic/chemokines and components of the MIF/CXC chemokine receptor axis, focusing on the influence of hypoxic versus normoxic stimulation. Hypoxia induced an upregulation of CXCR2 and CXCR4 but not CD74 on EPCs and triggered the secretion of CXCL12, CXCL1, MIF, and vascular endothelial growth factor (VEGF). These factors stimulated the transmigration activity and adhesive capacity of EPCs, with MIF and VEGF exhibiting the strongest effects under hypoxia. MIF-, VEGF-, CXCL12-, and CXCL1-stimulated EPCs enhanced tube formation, with MIF and VEGF exhibiting again the strongest effect following hypoxia. Tube formation following in vivo implantation utilizing angiogenic factor-loaded Matrigel plugs was only promoted by VEGF. Coloading of plugs with eEPCs led to enhanced tube formation only by CXCL12, whereas MIF was the only factor which induced differentiation towards an endothelial and smooth muscle cell (SMC) phenotype, indicating an angiogenic and differentiation capacity in vivo. Surprisingly, CXCL12, a chemoattractant for smooth muscle progenitor cells, inhibited SMC differentiation. We have identified a role for EPC-derived proangiogenic MIF, VEGF and MIF receptors in EPC recruitment following hypoxia, EPC differentiation and subsequent tube and vessel formation, whereas CXCL12, a mediator of early EPC recruitment, does not contribute to the remodeling process. By discerning the contributions of key angiogenic chemokines and EPCs, these findings offer valuable mechanistic insight into mouse models of angiogenesis and help to define the intricate interplay between EPC-derived angiogenic cargo factors, EPCs, and the angiogenic target tissue.
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         Macrophage migration inhibitory factor (MIF)
         Angiogenesis
         Hypoxia
         Embryonic endothelial progenitor cell (eEPC)
         Chemokine
         CXC
         Cardiology
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      name:Department of Cardiothoracic and Vascular Surgery, Johann Wolfgang Goethe-University, Frankfurt/Main, Germany
      name:Institute of Biochemistry and Molecular Cell Biology, Rheinisch-Westfälisch Technische Hochschule (RWTH) Aachen University, Aachen, Germany
      name:Institute for Molecular Cardiovascular Research (IMCAR), University Hospital, Rheinisch-Westfälisch Technische Hochschule (RWTH) Aachen University and Interdisciplinary Center for Clinical Research (IZKF), Aachen, Germany
      name:Institute of Biochemistry and Molecular Cell Biology, Rheinisch-Westfälisch Technische Hochschule (RWTH) Aachen University, Aachen, Germany
      name:Institute for Molecular Cardiovascular Research (IMCAR), University Hospital, Rheinisch-Westfälisch Technische Hochschule (RWTH) Aachen University and Interdisciplinary Center for Clinical Research (IZKF), Aachen, Germany
      name:Institute for Molecular Cardiovascular Research (IMCAR), University Hospital, Rheinisch-Westfälisch Technische Hochschule (RWTH) Aachen University and Interdisciplinary Center for Clinical Research (IZKF), Aachen, Germany
      name:Institute for Molecular Cardiovascular Research (IMCAR), University Hospital, Rheinisch-Westfälisch Technische Hochschule (RWTH) Aachen University and Interdisciplinary Center for Clinical Research (IZKF), Aachen, Germany
      name:Institute of Biochemistry and Molecular Cell Biology, Rheinisch-Westfälisch Technische Hochschule (RWTH) Aachen University, Aachen, Germany
      name:Department of Plastic Surgery and Hand and Burn Medicine, RWTH Aachen University, Aachen, Germany
      name:German Center for Cancer Research (DKFZ), Heidelberg, Germany
      name:Institute of Biochemistry and Molecular Cell Biology, Rheinisch-Westfälisch Technische Hochschule (RWTH) Aachen University, Aachen, Germany
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      name:Department of Internal Medicine, Yale University School of Medicine, New Haven, USA
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