Gr‐1+ CD 11b+ myeloid cells efficiently home to site of injury after intravenous administration and enhance diabetic wound healing by neoangiogenesis

Vascularization is an important factor that affects diabetic wound healing. There is increasing evidence that myeloid cell lineages play a role in neovascularization. In this study, the efficiency of Gr‐1+ CD 11b+ myeloid cells to home to the site of injury and enhance diabetic wound healing by neoa...

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Veröffentlicht in:Journal of cellular and molecular medicine 2014-06, Vol.18 (6), p.1194-1202
Hauptverfasser: Tong, Xiaozhe, Lv, Gang, Huang, Jianhua, Min, Yongfen, Yang, Li, Lin, Pengnian Charles
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Sprache:eng
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Zusammenfassung:Vascularization is an important factor that affects diabetic wound healing. There is increasing evidence that myeloid cell lineages play a role in neovascularization. In this study, the efficiency of Gr‐1+ CD 11b+ myeloid cells to home to the site of injury and enhance diabetic wound healing by neoangiogenesis after intravenous administration was investigated. Gr‐1+ CD 11b+ myeloid cells were injected into tail vein after establishment of dorsal window chamber, hindlimb ischaemia and ear‐punch injury in diabetic or non‐diabetic mice. The Gr‐1+ CD 11b+ myeloid cells efficiently homed to the site of injury after intravenous administration and increased neoangiogenesis. The chemokine receptor type 4 ( CXCR 4) is robustly expressed by Gr‐1+ CD 11b+ myeloid cells. Inhibition of CXCR 4 decreases the homing ability of Gr‐1+ CD 11b+ myeloid cells to the site of injury, which indicates that the CXCR 4/ SDF ‐1 axis plays an important role in the homing of Gr‐1+ CD 11b+ myeloid cells to the site of injury. In addition, Gr‐1+ CD 11b+ myeloid cells were found to improve blood flow recovery of ischaemic limb and enhance wound healing in diabetic mice by neoangiogenesis after intravenous administration. Taken together, the results of this study suggest that Gr‐1+ CD 11b+ myeloid cells may serve as a potential cell therapy for diabetic wound healing.
ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.12265