Open Access

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

Stem Cell Research & Therapy20178:50

https://doi.org/10.1186/s13287-017-0493-6

Received: 2 February 2017

Accepted: 3 February 2017

Published: 9 March 2017

The original article was published in Stem Cell Research & Therapy 2016 7:158

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]

Notes

Declarations

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’ Affiliations

(1)
Department of Pharmacology and Toxicology, University of Alabama at Birmingham School of Medicine
(2)
Department of Physiology, Laboratory for Vascular Medicine and Stem Cell Biology, Medical Research Institute, School of Medicine, Pusan National University
(3)
Research Institute of Convergence Biomedical Science and Technology, Pusan National University School of Medicine
(4)
Department of Immune Regulation, Research Centre for Hepatitis and Immunology, Research Institute, National Centre for Global Health and Medicine
(5)
Department of Regenerative Medicine Science, Tokai University School of Medicine
(6)
Division of Cardiology of Chonnam National University Hospital, Cardiovascular Convergence Research Center Nominated by Korea Ministry of Health and Welfare

Reference

  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/https://doi.org/10.1186/s13287-016-0403-3.View ArticleGoogle Scholar

Copyright

© The Author(s). 2017

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