Plerixafor stimulates adhesive activity and endothelial regeneration of endothelial progenitor cells via elevating CXCR7 expression |
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| Affiliation: | 1. Division of Pediatric Cardiology, Department of Pediatrics, University of Colorado – School of Medicine, Aurora, CO, United States of America;2. Section of Pediatric Endocrinology, Department of Pediatrics, University of Colorado – School of Medicine, Aurora, CO, United States of America;3. Section of Endocrinology, Rocky Mountain Regional VAMC, CO, United States of America;4. Division of Endocrinology, Department of Medicine, United States of America;5. Center for Women''s Health Research, University of Colorado – School of Medicine, Aurora, CO, United States of America;1. Department of Diabetes, King''s College NHS Foundation Trust, London, United Kingdom;2. King''s Health Partners'' Institute of Diabetes, Endocrinology and Obesity, London, UK;3. Department of Clinical and Experimental Medicine, University of Surrey, United Kingdom;4. Diabetes Centre-Diabetic Foot Clinic, Second Department of Internal Medicine, Democritus University of Thrace, Alexandroupolis, Greece |
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| Abstract: | AimsTo assess the effects of plerixafor on function and endothelial regeneration of endothelial progenitor cells (EPCs).MethodsThe proliferation and adhesion capacity of EPCs were evaluated in vitro. Furthermore, the expression levels of CXC chemokine receptor-7 (CXCR7) were detected before and after treatment with plerixafor. The CXCR7 expression of EPCs was knocked-down by RNA interference to evaluate the role of CXCR7 in regulating function of EPCs. A rat carotid artery injury model was established to assess the influences of plerixafor on endothelial regeneration.ResultsPlerixafor stimulated adhesion capacity of EPCs, associating with upregulation of CXCR7 and activation of LFA-1 and VLA-4 molecules. Knockdown of CXCR7 slightly impaired proliferation capacity but significantly attenuated adhesion capacity of EPCs. Plerixafor facilitated endothelial repair at 7 days, while reduced neointimal hyperplasia at 7 and 14 days via recruiting more EPCs participating in endothelial reparation.ConclusionsPlerixafor can positively regulate adhesion capacity of EPCs to HUVECs via elevating the expression level of CXCR7 and stimulating LFA-1 and VLA-4 molecules activation. Treatment with plerixafor accelerated re-endothelialization and inhibited neointimal hyperplasia after endoth elial injury, indicating that it can to be used for endothelial regeneration. |
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