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A Conditioned Medium of Umbilical Cord Mesenchymal Stem Cells Overexpressing Wnt7a Promotes Wound Repair and Regeneration of Hair Follicles in Mice

Mesenchymal stem cells (MSCs) can affect the microenvironment of a wound and thereby accelerate wound healing. Wnt proteins act as key mediators of skin development and participate in the formation of skin appendages such as hair. The mechanisms of action of MSCs and Wnt proteins on skin wounds are...

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Autores principales: Dong, Liang, Hao, Haojie, Liu, Jiejie, Ti, Dongdong, Tong, Chuan, Hou, Qian, Li, Meirong, Zheng, Jingxi, Liu, Gang, Fu, Xiaobing, Han, Weidong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350397/
https://www.ncbi.nlm.nih.gov/pubmed/28337222
http://dx.doi.org/10.1155/2017/3738071
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author Dong, Liang
Hao, Haojie
Liu, Jiejie
Ti, Dongdong
Tong, Chuan
Hou, Qian
Li, Meirong
Zheng, Jingxi
Liu, Gang
Fu, Xiaobing
Han, Weidong
author_facet Dong, Liang
Hao, Haojie
Liu, Jiejie
Ti, Dongdong
Tong, Chuan
Hou, Qian
Li, Meirong
Zheng, Jingxi
Liu, Gang
Fu, Xiaobing
Han, Weidong
author_sort Dong, Liang
collection PubMed
description Mesenchymal stem cells (MSCs) can affect the microenvironment of a wound and thereby accelerate wound healing. Wnt proteins act as key mediators of skin development and participate in the formation of skin appendages such as hair. The mechanisms of action of MSCs and Wnt proteins on skin wounds are largely unknown. Here, we prepared a Wnt7a-containing conditioned medium (Wnt-CM) from the supernatant of cultured human umbilical cord-MSCs (UC-MSCs) overexpressing Wnt7a in order to examine the effects of this CM on cutaneous healing. Our results revealed that Wnt-CM can accelerate wound closure and induce regeneration of hair follicles. Meanwhile, Wnt-CM enhanced expression of extracellular matrix (ECM) components and cell migration of fibroblasts but inhibited the migratory ability and expression of K6 and K16 in keratinocytes by enhancing expression of c-Myc. However, we found that the CM of fibroblasts treated with Wnt-CM (HF(Wnt-CM)-CM) can also promote wound repair and keratinocyte migration; but there was no increase in the number of hair follicles of regeneration. These data indicate that Wnt7a and UC-MSCs have synergistic effects: they can accelerate wound repair and induce hair regeneration via cellular communication in the wound microenvironment. Thus, this study opens up new avenues of research on the mechanisms underlying wound repair.
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spelling pubmed-53503972017-03-23 A Conditioned Medium of Umbilical Cord Mesenchymal Stem Cells Overexpressing Wnt7a Promotes Wound Repair and Regeneration of Hair Follicles in Mice Dong, Liang Hao, Haojie Liu, Jiejie Ti, Dongdong Tong, Chuan Hou, Qian Li, Meirong Zheng, Jingxi Liu, Gang Fu, Xiaobing Han, Weidong Stem Cells Int Research Article Mesenchymal stem cells (MSCs) can affect the microenvironment of a wound and thereby accelerate wound healing. Wnt proteins act as key mediators of skin development and participate in the formation of skin appendages such as hair. The mechanisms of action of MSCs and Wnt proteins on skin wounds are largely unknown. Here, we prepared a Wnt7a-containing conditioned medium (Wnt-CM) from the supernatant of cultured human umbilical cord-MSCs (UC-MSCs) overexpressing Wnt7a in order to examine the effects of this CM on cutaneous healing. Our results revealed that Wnt-CM can accelerate wound closure and induce regeneration of hair follicles. Meanwhile, Wnt-CM enhanced expression of extracellular matrix (ECM) components and cell migration of fibroblasts but inhibited the migratory ability and expression of K6 and K16 in keratinocytes by enhancing expression of c-Myc. However, we found that the CM of fibroblasts treated with Wnt-CM (HF(Wnt-CM)-CM) can also promote wound repair and keratinocyte migration; but there was no increase in the number of hair follicles of regeneration. These data indicate that Wnt7a and UC-MSCs have synergistic effects: they can accelerate wound repair and induce hair regeneration via cellular communication in the wound microenvironment. Thus, this study opens up new avenues of research on the mechanisms underlying wound repair. Hindawi Publishing Corporation 2017 2017-02-27 /pmc/articles/PMC5350397/ /pubmed/28337222 http://dx.doi.org/10.1155/2017/3738071 Text en Copyright © 2017 Liang Dong et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Dong, Liang
Hao, Haojie
Liu, Jiejie
Ti, Dongdong
Tong, Chuan
Hou, Qian
Li, Meirong
Zheng, Jingxi
Liu, Gang
Fu, Xiaobing
Han, Weidong
A Conditioned Medium of Umbilical Cord Mesenchymal Stem Cells Overexpressing Wnt7a Promotes Wound Repair and Regeneration of Hair Follicles in Mice
title A Conditioned Medium of Umbilical Cord Mesenchymal Stem Cells Overexpressing Wnt7a Promotes Wound Repair and Regeneration of Hair Follicles in Mice
title_full A Conditioned Medium of Umbilical Cord Mesenchymal Stem Cells Overexpressing Wnt7a Promotes Wound Repair and Regeneration of Hair Follicles in Mice
title_fullStr A Conditioned Medium of Umbilical Cord Mesenchymal Stem Cells Overexpressing Wnt7a Promotes Wound Repair and Regeneration of Hair Follicles in Mice
title_full_unstemmed A Conditioned Medium of Umbilical Cord Mesenchymal Stem Cells Overexpressing Wnt7a Promotes Wound Repair and Regeneration of Hair Follicles in Mice
title_short A Conditioned Medium of Umbilical Cord Mesenchymal Stem Cells Overexpressing Wnt7a Promotes Wound Repair and Regeneration of Hair Follicles in Mice
title_sort conditioned medium of umbilical cord mesenchymal stem cells overexpressing wnt7a promotes wound repair and regeneration of hair follicles in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350397/
https://www.ncbi.nlm.nih.gov/pubmed/28337222
http://dx.doi.org/10.1155/2017/3738071
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