The mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery.
Delayed wound healing is a serious clinical problem in patients after surgery. A recent study has demonstrated that bone marrow-derived c-kit-positive (c-kit(+)) cells play important roles in repairing and regenerating various tissues and organs. To examine the hypothesis that surgical injury induce...
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2012
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oai:doaj.org-article:a7e46c66a99d41cd9e98afaa41b5a8e92021-11-18T08:08:56ZThe mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery.1932-620310.1371/journal.pone.0048052https://doaj.org/article/a7e46c66a99d41cd9e98afaa41b5a8e92012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23155375/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Delayed wound healing is a serious clinical problem in patients after surgery. A recent study has demonstrated that bone marrow-derived c-kit-positive (c-kit(+)) cells play important roles in repairing and regenerating various tissues and organs. To examine the hypothesis that surgical injury induces the mobilization and recruitment of c-kit+ cells to accelerate wound healing. Mice were subjected to a left pneumonectomy. The mobilization of c-kit+ cells was monitored after surgery. Using green fluorescent protein (GFP(+)) bone marrow-transplanted chimera mice, we investigated further whether the mobilized c-kit+ cells were recruited to effect wound healing in a skin puncture model. The group with left pneumonectomies increased the c-kit(+) and CD34(+) stem cells in peripheral blood 24 h after surgery. At 3 days after surgery, the skin wound size was observed to be significantly smaller, and the number of bone marrow-derived GFP(+) cells and GFP(+)/c-kit+ cells in the wound tissue was significantly greater in mice that had received pneumonectomies, as compared with those that had received a sham operation. Furthermore, some of these GFP(+) cells were positively expressed specific markers of macrophages (F4/80), endothelial cells (CD31), and myofibroblasts (αSMA). The administration of AMD3100, an antagonist of a stromal-cell derived factor (SDF)-1/CXCR4 signaling pathway, reduced the number of GFP(+) cells in wound tissue and completely negated the accelerated wound healing. Surgical injury induces the mobilization and recruitment of c-kit+ cells to contribute to wound healing. Regulating c-kit+ cells may provide a new approach that accelerates wound healing after surgery.Yoshihiro TakemotoTao-Sheng LiMasayuki KuboMako OhshimaHiroshi KurazumiKazuhiro UedaTadahiko EnokiTomoaki MurataKimikazu HamanoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 11, p e48052 (2012) |
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Medicine R Science Q Yoshihiro Takemoto Tao-Sheng Li Masayuki Kubo Mako Ohshima Hiroshi Kurazumi Kazuhiro Ueda Tadahiko Enoki Tomoaki Murata Kimikazu Hamano The mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery. |
description |
Delayed wound healing is a serious clinical problem in patients after surgery. A recent study has demonstrated that bone marrow-derived c-kit-positive (c-kit(+)) cells play important roles in repairing and regenerating various tissues and organs. To examine the hypothesis that surgical injury induces the mobilization and recruitment of c-kit+ cells to accelerate wound healing. Mice were subjected to a left pneumonectomy. The mobilization of c-kit+ cells was monitored after surgery. Using green fluorescent protein (GFP(+)) bone marrow-transplanted chimera mice, we investigated further whether the mobilized c-kit+ cells were recruited to effect wound healing in a skin puncture model. The group with left pneumonectomies increased the c-kit(+) and CD34(+) stem cells in peripheral blood 24 h after surgery. At 3 days after surgery, the skin wound size was observed to be significantly smaller, and the number of bone marrow-derived GFP(+) cells and GFP(+)/c-kit+ cells in the wound tissue was significantly greater in mice that had received pneumonectomies, as compared with those that had received a sham operation. Furthermore, some of these GFP(+) cells were positively expressed specific markers of macrophages (F4/80), endothelial cells (CD31), and myofibroblasts (αSMA). The administration of AMD3100, an antagonist of a stromal-cell derived factor (SDF)-1/CXCR4 signaling pathway, reduced the number of GFP(+) cells in wound tissue and completely negated the accelerated wound healing. Surgical injury induces the mobilization and recruitment of c-kit+ cells to contribute to wound healing. Regulating c-kit+ cells may provide a new approach that accelerates wound healing after surgery. |
format |
article |
author |
Yoshihiro Takemoto Tao-Sheng Li Masayuki Kubo Mako Ohshima Hiroshi Kurazumi Kazuhiro Ueda Tadahiko Enoki Tomoaki Murata Kimikazu Hamano |
author_facet |
Yoshihiro Takemoto Tao-Sheng Li Masayuki Kubo Mako Ohshima Hiroshi Kurazumi Kazuhiro Ueda Tadahiko Enoki Tomoaki Murata Kimikazu Hamano |
author_sort |
Yoshihiro Takemoto |
title |
The mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery. |
title_short |
The mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery. |
title_full |
The mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery. |
title_fullStr |
The mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery. |
title_full_unstemmed |
The mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery. |
title_sort |
mobilization and recruitment of c-kit+ cells contribute to wound healing after surgery. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2012 |
url |
https://doaj.org/article/a7e46c66a99d41cd9e98afaa41b5a8e9 |
work_keys_str_mv |
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