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miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7
Both the miR-17-92 cluster and autophagy have been suggested as critical regulators of bone development, but the potential correlation between the two factors is largely unknown. Hence, we investigated whether members of this cluster can regulate chondrogenesis through an autophagy-related signallin...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6592888/ https://www.ncbi.nlm.nih.gov/pubmed/31239522 http://dx.doi.org/10.1038/s41598-019-45502-7 |
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author | Xu, Rui Wei, Yuhao Yin, Xing Shi, Bing Li, Jingtao |
author_facet | Xu, Rui Wei, Yuhao Yin, Xing Shi, Bing Li, Jingtao |
author_sort | Xu, Rui |
collection | PubMed |
description | Both the miR-17-92 cluster and autophagy have been suggested as critical regulators of bone development, but the potential correlation between the two factors is largely unknown. Hence, we investigated whether members of this cluster can regulate chondrogenesis through an autophagy-related signalling pathway. In this study, the expression of miR-17-92 cluster members and the level of autophagic activity were investigated during chondrogenic induction in ATDC5 cells. miR-17, miR-18a, miR-20a, and miR-92-1 showed significant changes, and the level of autophagic activity was enhanced. Among the miR-17-92 cluster members, miR-20a showed the most significant change. Histological, cellular and molecular analyses were performed after the regulation of miR-20a and autophagy. miR-20a and autophagy had the opposite effect on chondrogenic differentiation, and there was a negative correlation between them. Moreover, the expression of the autophagy regulatory gene Atg7 was inhibited by miR-20a. siRNA was then used to knock down Atg7, and the results further indicated that Atg7 might be a potential target of miR-20a in chondrogenic differentiation. In conclusion, miR-20a is a critical negative regulator of chondrogenic differentiation because it inhibits autophagy via Atg7. Other members of the miR-17-92 cluster may have a similar effect, but this hypothesis requires further investigation. |
format | Online Article Text |
id | pubmed-6592888 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-65928882019-07-03 miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7 Xu, Rui Wei, Yuhao Yin, Xing Shi, Bing Li, Jingtao Sci Rep Article Both the miR-17-92 cluster and autophagy have been suggested as critical regulators of bone development, but the potential correlation between the two factors is largely unknown. Hence, we investigated whether members of this cluster can regulate chondrogenesis through an autophagy-related signalling pathway. In this study, the expression of miR-17-92 cluster members and the level of autophagic activity were investigated during chondrogenic induction in ATDC5 cells. miR-17, miR-18a, miR-20a, and miR-92-1 showed significant changes, and the level of autophagic activity was enhanced. Among the miR-17-92 cluster members, miR-20a showed the most significant change. Histological, cellular and molecular analyses were performed after the regulation of miR-20a and autophagy. miR-20a and autophagy had the opposite effect on chondrogenic differentiation, and there was a negative correlation between them. Moreover, the expression of the autophagy regulatory gene Atg7 was inhibited by miR-20a. siRNA was then used to knock down Atg7, and the results further indicated that Atg7 might be a potential target of miR-20a in chondrogenic differentiation. In conclusion, miR-20a is a critical negative regulator of chondrogenic differentiation because it inhibits autophagy via Atg7. Other members of the miR-17-92 cluster may have a similar effect, but this hypothesis requires further investigation. Nature Publishing Group UK 2019-06-25 /pmc/articles/PMC6592888/ /pubmed/31239522 http://dx.doi.org/10.1038/s41598-019-45502-7 Text en © The Author(s) 2019 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 Xu, Rui Wei, Yuhao Yin, Xing Shi, Bing Li, Jingtao miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7 |
title | miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7 |
title_full | miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7 |
title_fullStr | miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7 |
title_full_unstemmed | miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7 |
title_short | miR-20a suppresses chondrogenic differentiation of ATDC5 cells by regulating Atg7 |
title_sort | mir-20a suppresses chondrogenic differentiation of atdc5 cells by regulating atg7 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6592888/ https://www.ncbi.nlm.nih.gov/pubmed/31239522 http://dx.doi.org/10.1038/s41598-019-45502-7 |
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