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Autophagy promotes MSC-mediated vascularization in cutaneous wound healing via regulation of VEGF secretion
Vascularization deficiency caused a lot of diseases, such as diabetes ulcer and myocardial infarction. Mesenchymal stem cells (MSCs), with the self-renewal and multipotent differentiation capacities, have been used for many diseases treatment through regulation microenvironment. Numerous studies rep...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5833357/ https://www.ncbi.nlm.nih.gov/pubmed/29352190 http://dx.doi.org/10.1038/s41419-017-0082-8 |
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author | An, Y. Liu, W. J. Xue, P. Ma, Y. Zhang, L. Q. Zhu, B. Qi, M. Li, L. Y. Zhang, Y. J. Wang, Q. T. Jin, Y. |
author_facet | An, Y. Liu, W. J. Xue, P. Ma, Y. Zhang, L. Q. Zhu, B. Qi, M. Li, L. Y. Zhang, Y. J. Wang, Q. T. Jin, Y. |
author_sort | An, Y. |
collection | PubMed |
description | Vascularization deficiency caused a lot of diseases, such as diabetes ulcer and myocardial infarction. Mesenchymal stem cells (MSCs), with the self-renewal and multipotent differentiation capacities, have been used for many diseases treatment through regulation microenvironment. Numerous studies reported that MSCs transplantation could largely improve cutaneous wound healing via paracrine secretion of growth factors. However, whether MSCs take part in the angiogenesis process directly remains elusive. Previous study proved that autophagy inhibited immunosuppressive function of MSCs and prevented the degradation of MSCs function in inflammatory and senescent microenvironment. Here, we proved that autophagy determines the therapeutic effect of MSCs in cutaneous wound healing through promoting endothelial cells angiogenesis and demonstrated that the paracrine of vascular endothelial growth factor (VEGF) in MSCs was required in wound site. We further revealed that autophagy enhanced the VEGF secretion from MSCs through ERK phosphorylation directly. Collectively, we put forward that autophagy mediated paracrine of VEGF plays a central role in MSCs cured cutaneous wound healing and may provide a new therapeutic method for angiogenesis-related diseases. |
format | Online Article Text |
id | pubmed-5833357 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58333572018-03-05 Autophagy promotes MSC-mediated vascularization in cutaneous wound healing via regulation of VEGF secretion An, Y. Liu, W. J. Xue, P. Ma, Y. Zhang, L. Q. Zhu, B. Qi, M. Li, L. Y. Zhang, Y. J. Wang, Q. T. Jin, Y. Cell Death Dis Article Vascularization deficiency caused a lot of diseases, such as diabetes ulcer and myocardial infarction. Mesenchymal stem cells (MSCs), with the self-renewal and multipotent differentiation capacities, have been used for many diseases treatment through regulation microenvironment. Numerous studies reported that MSCs transplantation could largely improve cutaneous wound healing via paracrine secretion of growth factors. However, whether MSCs take part in the angiogenesis process directly remains elusive. Previous study proved that autophagy inhibited immunosuppressive function of MSCs and prevented the degradation of MSCs function in inflammatory and senescent microenvironment. Here, we proved that autophagy determines the therapeutic effect of MSCs in cutaneous wound healing through promoting endothelial cells angiogenesis and demonstrated that the paracrine of vascular endothelial growth factor (VEGF) in MSCs was required in wound site. We further revealed that autophagy enhanced the VEGF secretion from MSCs through ERK phosphorylation directly. Collectively, we put forward that autophagy mediated paracrine of VEGF plays a central role in MSCs cured cutaneous wound healing and may provide a new therapeutic method for angiogenesis-related diseases. Nature Publishing Group UK 2018-01-19 /pmc/articles/PMC5833357/ /pubmed/29352190 http://dx.doi.org/10.1038/s41419-017-0082-8 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article An, Y. Liu, W. J. Xue, P. Ma, Y. Zhang, L. Q. Zhu, B. Qi, M. Li, L. Y. Zhang, Y. J. Wang, Q. T. Jin, Y. Autophagy promotes MSC-mediated vascularization in cutaneous wound healing via regulation of VEGF secretion |
title | Autophagy promotes MSC-mediated vascularization in cutaneous wound healing via regulation of VEGF secretion |
title_full | Autophagy promotes MSC-mediated vascularization in cutaneous wound healing via regulation of VEGF secretion |
title_fullStr | Autophagy promotes MSC-mediated vascularization in cutaneous wound healing via regulation of VEGF secretion |
title_full_unstemmed | Autophagy promotes MSC-mediated vascularization in cutaneous wound healing via regulation of VEGF secretion |
title_short | Autophagy promotes MSC-mediated vascularization in cutaneous wound healing via regulation of VEGF secretion |
title_sort | autophagy promotes msc-mediated vascularization in cutaneous wound healing via regulation of vegf secretion |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5833357/ https://www.ncbi.nlm.nih.gov/pubmed/29352190 http://dx.doi.org/10.1038/s41419-017-0082-8 |
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