The role of fucosylation in the promotion of endothelial progenitor cells in neovascularization and bone repair |
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| Authors: | Shengxuan Sun Zhenzhen Liu Haibin Zhou Guoqiang Li Meng Liu Jiannan Yao Tiantian Zhou Guangyu An Qingyu Wu Ningzheng Dong |
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| Affiliation: | 1. The Cyrus Tang Hematology Center, Soochow University, Suzhou 215123, China;2. The Second Affiliated Hospital, Soochow University, Suzhou 215004, China;3. Department of Oncology, Chao-Yang Hospital, Capital Medical University, Beijing 100020, China;4. Molecular Cardiology, Cleveland Clinic, Cleveland, OH 44195, USA;5. The MOH Key Laboratory of Thrombosis and Hemostasis, Jiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China |
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| Abstract: | Bone marrow-derived endothelial progenitor cells (EPCs) are being tested as a therapy to treat a variety of ischemic diseases. Poor homing to targeted tissues is one of the major factors limiting the therapeutic efficacy of EPCs. Here, we show that human cord blood-derived EPCs expressed little sialyl Lewis X (sLex) antigen that is necessary for selectin-mediated cell–cell interactions. Expression of α1,3-fucosyltransferase VI (FucT VI) in the EPCs enhanced sLex synthesis, E- and P-selectin-binding, and EPC adhesion to tumor necrosis factor-α-stimulated human umbilical vein endothelial cells in culture. In a mouse model of hind limb ischemia, in which EPCs were injected intravenously, FucT VI expression increased EPC homing, neovascularization, and blood flow in ischemic muscles. In another mouse model of femoral fracture, FucT VI-expressing EPCs were more efficient than control EPCs in targeting to peri-fracture tissues to enhance angiogenesis, blood flow and bone repair. These results indicate that fucosylated EPCs may be used to as an improved cellular source to treat ischemic diseases. |
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| Keywords: | Angiogenesis Bone repair Endothelial progenitor cells Fucosylation Ischemic disease Selectins |
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