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. 2017 Feb 7;8:29. doi: 10.1186/s13287-017-0470-0

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — DFO treatment enhanced gene expression of Flk and vWF (a). eELCs showed higher wound closure ability (%) than MSCs in normoxia (DFO = 0), and hypoxia (DFO) further increased the closure performance in a dose-dependent manner (b). CXCR4 gene expression was increased after treating eELCs with DFO for 24 hr (c). Scale bar: 200 μm. *Significant from the same cell under regular culture condition (without DFO), p < 0.05; #significant from MSCs under the same treatment, p < 0.05. DFO desferrioxamine, MSC mesenchymal stem cells, eELC early endothelial lineage cells, vWF von Willebrand factor, SDF-1 stromal cell-derived factor-1, CXCR4 C-X-C chemokine receptor type 4