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Autophagy modulates mesenchymal-to-endothelial transition via p53
Mesenchymal-to-endothelial transition (MEndT) is one of the mechanisms that influences cardiac fibrosis, which is a key process in cardiac remodeling. It has been reported that autophagy inhibits endothelial cell transition. However, whether autophagy could modulate MEndT in cardiac fibrosis has not...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695417/ https://www.ncbi.nlm.nih.gov/pubmed/33186920 http://dx.doi.org/10.18632/aging.104065 |
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author | Hu, Jie Kong, Shuting Dong, Tiancheng Lin, Zhiwei Zhang, Qihao Chen, Xingxing Gong, Yongsheng Fan, Xiaofang He, Mingyu Zhou, Hao |
author_facet | Hu, Jie Kong, Shuting Dong, Tiancheng Lin, Zhiwei Zhang, Qihao Chen, Xingxing Gong, Yongsheng Fan, Xiaofang He, Mingyu Zhou, Hao |
author_sort | Hu, Jie |
collection | PubMed |
description | Mesenchymal-to-endothelial transition (MEndT) is one of the mechanisms that influences cardiac fibrosis, which is a key process in cardiac remodeling. It has been reported that autophagy inhibits endothelial cell transition. However, whether autophagy could modulate MEndT in cardiac fibrosis has not yet been investigated. Here, we discussed the association between autophagy and MEndT and its possible mechanism. In this study, we induced endothelial-to-mesenchymal transition using transforming growth factor-β to generate mesenchymal cells and fibroblasts in wild-type human umbilical vein endothelial cells and cells with p53 knockout or overexpression. Then, autophagy was induced by Earle's balanced salt solution (EBSS) and was inhibited by bafilomycin A1 or lentivirus-ATG5-shRNA. The expression levels of MEndT and the autophagy markers CD31, VE-Cadherin, Vimentin, α-SMA, LC3, p62 and p53 were examined. We found that activation of autophagy could promote MEndT and increase cytoplasmic and total expression of p53, that but nuclear p53 expression was decreased, and that inhibition of autophagy activation could reverse the effect of EBSS. Moreover, after knockout of nuclear p53, autophagy promoted MEndT, while autophagy inhibited MEndT in p53 overexpressing cells. Our results demonstrate that autophagy modulate MEndT by nuclear p53 provide a new strategy for the treatment of fibrosis diseases. |
format | Online Article Text |
id | pubmed-7695417 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-76954172020-12-04 Autophagy modulates mesenchymal-to-endothelial transition via p53 Hu, Jie Kong, Shuting Dong, Tiancheng Lin, Zhiwei Zhang, Qihao Chen, Xingxing Gong, Yongsheng Fan, Xiaofang He, Mingyu Zhou, Hao Aging (Albany NY) Research Paper Mesenchymal-to-endothelial transition (MEndT) is one of the mechanisms that influences cardiac fibrosis, which is a key process in cardiac remodeling. It has been reported that autophagy inhibits endothelial cell transition. However, whether autophagy could modulate MEndT in cardiac fibrosis has not yet been investigated. Here, we discussed the association between autophagy and MEndT and its possible mechanism. In this study, we induced endothelial-to-mesenchymal transition using transforming growth factor-β to generate mesenchymal cells and fibroblasts in wild-type human umbilical vein endothelial cells and cells with p53 knockout or overexpression. Then, autophagy was induced by Earle's balanced salt solution (EBSS) and was inhibited by bafilomycin A1 or lentivirus-ATG5-shRNA. The expression levels of MEndT and the autophagy markers CD31, VE-Cadherin, Vimentin, α-SMA, LC3, p62 and p53 were examined. We found that activation of autophagy could promote MEndT and increase cytoplasmic and total expression of p53, that but nuclear p53 expression was decreased, and that inhibition of autophagy activation could reverse the effect of EBSS. Moreover, after knockout of nuclear p53, autophagy promoted MEndT, while autophagy inhibited MEndT in p53 overexpressing cells. Our results demonstrate that autophagy modulate MEndT by nuclear p53 provide a new strategy for the treatment of fibrosis diseases. Impact Journals 2020-11-13 /pmc/articles/PMC7695417/ /pubmed/33186920 http://dx.doi.org/10.18632/aging.104065 Text en Copyright: © 2020 Hu et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Hu, Jie Kong, Shuting Dong, Tiancheng Lin, Zhiwei Zhang, Qihao Chen, Xingxing Gong, Yongsheng Fan, Xiaofang He, Mingyu Zhou, Hao Autophagy modulates mesenchymal-to-endothelial transition via p53 |
title | Autophagy modulates mesenchymal-to-endothelial transition via p53 |
title_full | Autophagy modulates mesenchymal-to-endothelial transition via p53 |
title_fullStr | Autophagy modulates mesenchymal-to-endothelial transition via p53 |
title_full_unstemmed | Autophagy modulates mesenchymal-to-endothelial transition via p53 |
title_short | Autophagy modulates mesenchymal-to-endothelial transition via p53 |
title_sort | autophagy modulates mesenchymal-to-endothelial transition via p53 |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695417/ https://www.ncbi.nlm.nih.gov/pubmed/33186920 http://dx.doi.org/10.18632/aging.104065 |
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