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Erratum to: Specific disruption of Lnk in murine endothelial progenitor cells promotes dermal wound healing via enhanced vasculogenesis, activation of myofibroblasts, and suppression of inflammatory cell recruitment

  • Jun Hee Lee
  • Seung Taek Ji
  • Jaeho Kim
  • Satoshi Takaki
  • Takayuki Asahara
  • Young-Joon Hong
  • Sang-Mo Kwon
Open Access
Erratum
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Erratum

Unfortunately, after publication of this article [1], it was noticed that Fig. 4 was incorrect. Panels B and D contained incorrect graphs. The corrected Fig. 4 can be seen below and the original article has been updated to correct this.
Fig. 4

A transplant of Lnk-deficient EPCs suppresses the recruitment of inflammatory cells. After injection of wild-type (WT) and Lnk-deficient EPCs into wound sites, wound tissues were analyzed to determine the recruitment of cytotoxic T cells (CD3- and CD8-positive cells), macrophages (CD11b-positive cells), and neutrophils (CD45-positive cells) on postoperative days 3 and 7. a The recruitment of cytotoxic T cells in wound tissues was assessed by FACS analysis. b The percentage of CD3/CD8 double-positive cells on postoperative days 3 and 7. Values are mean ± SEM; **p < 0.01 compared to postoperative day 3, respectively, and ##p < 0.01 compared to injection with WT EPCs. c The recruitment of macrophages and neutrophils to wound tissues was assessed by FACS analysis. d The percentage of CD11b- and CD45-positive cells on postoperative days 3 and 7. Values are mean ± SEM;**p < 0.01 compared to postoperative day 3, respectively, #p < 0.05 and ##p < 0.01 compared to injection with WT EPCs]

Reference

  1. 1.
    Lee JH, Ji ST, Kim J, Takaki S, Asahara T, Hong Y-J, Kwon S-M. Specific disruption of Lnk in murine endothelial progenitor cells promotes dermal wound healing via enhanced vasculogenesis, activation of myofibroblasts, and suppression of inflammatory cell recruitment. Stem Cell Research & Therapy. 2016;7:158. http://doi.org/ 10.1186/s13287-016-0403-3.CrossRefGoogle Scholar

Copyright information

© 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.

Authors and Affiliations

  • Jun Hee Lee
    • 1
  • Seung Taek Ji
    • 2
  • Jaeho Kim
    • 3
  • Satoshi Takaki
    • 4
  • Takayuki Asahara
    • 5
  • Young-Joon Hong
    • 6
  • Sang-Mo Kwon
    • 2
  1. 1.Department of Pharmacology and ToxicologyUniversity of Alabama at Birmingham School of MedicineBirminghamUSA
  2. 2.Department of Physiology, Laboratory for Vascular Medicine and Stem Cell Biology, Medical Research Institute, School of MedicinePusan National UniversityYangsanRepublic of Korea
  3. 3.Research Institute of Convergence Biomedical Science and TechnologyPusan National University School of MedicineYangsanRepublic of Korea
  4. 4.Department of Immune Regulation, Research Centre for Hepatitis and Immunology, Research Institute, National Centre for Global Health and MedicineChibaJapan
  5. 5.Department of Regenerative Medicine ScienceTokai University School of MedicineKanagawaJapan
  6. 6.Division of Cardiology of Chonnam National University Hospital, Cardiovascular Convergence Research Center Nominated by Korea Ministry of Health and WelfareGwangjuRepublic of Korea

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