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Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling
Adiponectin has been demonstrated to protect the cardiovascular system and bone marrow mesenchymal stem cells (BMSCs). However, it is unclear whether adiponectin can protect BMSCs against flow shear stress (FSS). In this study, our aim was to explore the effects of adiponectin on BMSCs and to explor...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4945870/ https://www.ncbi.nlm.nih.gov/pubmed/27418435 http://dx.doi.org/10.1038/srep28752 |
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author | Zhao, Lin Fan, Chongxi Zhang, Yu Yang, Yang Wang, Dongjin Deng, Chao Hu, Wei Ma, Zhiqiang Jiang, Shuai Di, Shouyi Qin, Zhigang Lv, Jianjun Sun, Yang Yi, Wei |
author_facet | Zhao, Lin Fan, Chongxi Zhang, Yu Yang, Yang Wang, Dongjin Deng, Chao Hu, Wei Ma, Zhiqiang Jiang, Shuai Di, Shouyi Qin, Zhigang Lv, Jianjun Sun, Yang Yi, Wei |
author_sort | Zhao, Lin |
collection | PubMed |
description | Adiponectin has been demonstrated to protect the cardiovascular system and bone marrow mesenchymal stem cells (BMSCs). However, it is unclear whether adiponectin can protect BMSCs against flow shear stress (FSS). In this study, our aim was to explore the effects of adiponectin on BMSCs and to explore the role of AMP-activated protein kinase (AMPK) signaling in this process. Shear stress significantly inhibits the survival and increases the apoptosis of BMSCs in an intensity-dependent manner. The expression levels of TGF-β, bFGF, VEGF, PDGF, and Bcl2 are simultaneously reduced, and the phosphorylation levels of AMPK and ACC, as well as the expression level of Bax, are increased. Supplementation with adiponectin promotes the survival of BMSCs; reverses the changes in the expression levels of TGF-β, bFGF, VEGF, PDGF, Bcl2, and Bax; and further amplifies the phosphorylation of AMPK and ACC. Furthermore, the protective effects of adiponectin can be partially neutralized by AMPK siRNA. In summary, we have demonstrated for the first time that adiponectin can effectively protect BMSCs from FSS and that this effect depends, at least in part, on the activation of AMPK signaling. |
format | Online Article Text |
id | pubmed-4945870 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49458702016-07-26 Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling Zhao, Lin Fan, Chongxi Zhang, Yu Yang, Yang Wang, Dongjin Deng, Chao Hu, Wei Ma, Zhiqiang Jiang, Shuai Di, Shouyi Qin, Zhigang Lv, Jianjun Sun, Yang Yi, Wei Sci Rep Article Adiponectin has been demonstrated to protect the cardiovascular system and bone marrow mesenchymal stem cells (BMSCs). However, it is unclear whether adiponectin can protect BMSCs against flow shear stress (FSS). In this study, our aim was to explore the effects of adiponectin on BMSCs and to explore the role of AMP-activated protein kinase (AMPK) signaling in this process. Shear stress significantly inhibits the survival and increases the apoptosis of BMSCs in an intensity-dependent manner. The expression levels of TGF-β, bFGF, VEGF, PDGF, and Bcl2 are simultaneously reduced, and the phosphorylation levels of AMPK and ACC, as well as the expression level of Bax, are increased. Supplementation with adiponectin promotes the survival of BMSCs; reverses the changes in the expression levels of TGF-β, bFGF, VEGF, PDGF, Bcl2, and Bax; and further amplifies the phosphorylation of AMPK and ACC. Furthermore, the protective effects of adiponectin can be partially neutralized by AMPK siRNA. In summary, we have demonstrated for the first time that adiponectin can effectively protect BMSCs from FSS and that this effect depends, at least in part, on the activation of AMPK signaling. Nature Publishing Group 2016-07-15 /pmc/articles/PMC4945870/ /pubmed/27418435 http://dx.doi.org/10.1038/srep28752 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Zhao, Lin Fan, Chongxi Zhang, Yu Yang, Yang Wang, Dongjin Deng, Chao Hu, Wei Ma, Zhiqiang Jiang, Shuai Di, Shouyi Qin, Zhigang Lv, Jianjun Sun, Yang Yi, Wei Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling |
title | Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling |
title_full | Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling |
title_fullStr | Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling |
title_full_unstemmed | Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling |
title_short | Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling |
title_sort | adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through amp-activated protein kinase signaling |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4945870/ https://www.ncbi.nlm.nih.gov/pubmed/27418435 http://dx.doi.org/10.1038/srep28752 |
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