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Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1
Lung fibrosis, including idiopathic pulmonary fibrosis, is an intractable disease accompanied by an irreversible dysfunction in the respiratory system. Its pathogenesis involves the transforming growth factorβ (TGFβ)-induced overproduction of the extracellular matrix from fibroblasts; however, limit...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9901827/ https://www.ncbi.nlm.nih.gov/pubmed/36746980 http://dx.doi.org/10.1038/s41598-023-29188-6 |
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author | Kumazoe, Motofumi Ogawa, Fumiyo Hikida, Ai Shimada, Yu Yoshitomi, Ren Watanabe, Ryoya Onda, Hiroaki Fujimura, Yoshinori Tachibana, Hirofumi |
author_facet | Kumazoe, Motofumi Ogawa, Fumiyo Hikida, Ai Shimada, Yu Yoshitomi, Ren Watanabe, Ryoya Onda, Hiroaki Fujimura, Yoshinori Tachibana, Hirofumi |
author_sort | Kumazoe, Motofumi |
collection | PubMed |
description | Lung fibrosis, including idiopathic pulmonary fibrosis, is an intractable disease accompanied by an irreversible dysfunction in the respiratory system. Its pathogenesis involves the transforming growth factorβ (TGFβ)-induced overproduction of the extracellular matrix from fibroblasts; however, limited countermeasures have been established. In this study, we identified osa-miR172d-5p, a plant-derived microRNA (miR), as a potent anti-fibrotic miR. In silico analysis followed by an in vitro assay based on human lung fibroblasts demonstrated that osa-miR172d-5p suppressed the gene expression of TGF-β activated kinase 1 (MAP3K7) binding protein 1 (Tab1). It also suppressed the TGFβ-induced fibrotic gene expression in human lung fibroblasts. To assess the anti-fibrotic effect of osa-miR172d-5p, we established bleomycin-induced lung fibrosis models to demonstrate that osa-miR172d-5p ameliorated lung fibrosis. Moreover, it suppressed Tab1 expression in the lung tissues of bleomycin-treated mice. In conclusion, osa-miR172d-5p could be a potent candidate for the treatment of lung fibrosis, including idiopathic pulmonary fibrosis. |
format | Online Article Text |
id | pubmed-9901827 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-99018272023-02-07 Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1 Kumazoe, Motofumi Ogawa, Fumiyo Hikida, Ai Shimada, Yu Yoshitomi, Ren Watanabe, Ryoya Onda, Hiroaki Fujimura, Yoshinori Tachibana, Hirofumi Sci Rep Article Lung fibrosis, including idiopathic pulmonary fibrosis, is an intractable disease accompanied by an irreversible dysfunction in the respiratory system. Its pathogenesis involves the transforming growth factorβ (TGFβ)-induced overproduction of the extracellular matrix from fibroblasts; however, limited countermeasures have been established. In this study, we identified osa-miR172d-5p, a plant-derived microRNA (miR), as a potent anti-fibrotic miR. In silico analysis followed by an in vitro assay based on human lung fibroblasts demonstrated that osa-miR172d-5p suppressed the gene expression of TGF-β activated kinase 1 (MAP3K7) binding protein 1 (Tab1). It also suppressed the TGFβ-induced fibrotic gene expression in human lung fibroblasts. To assess the anti-fibrotic effect of osa-miR172d-5p, we established bleomycin-induced lung fibrosis models to demonstrate that osa-miR172d-5p ameliorated lung fibrosis. Moreover, it suppressed Tab1 expression in the lung tissues of bleomycin-treated mice. In conclusion, osa-miR172d-5p could be a potent candidate for the treatment of lung fibrosis, including idiopathic pulmonary fibrosis. Nature Publishing Group UK 2023-02-06 /pmc/articles/PMC9901827/ /pubmed/36746980 http://dx.doi.org/10.1038/s41598-023-29188-6 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Kumazoe, Motofumi Ogawa, Fumiyo Hikida, Ai Shimada, Yu Yoshitomi, Ren Watanabe, Ryoya Onda, Hiroaki Fujimura, Yoshinori Tachibana, Hirofumi Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1 |
title | Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1 |
title_full | Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1 |
title_fullStr | Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1 |
title_full_unstemmed | Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1 |
title_short | Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1 |
title_sort | plant mirna osa-mir172d-5p suppressed lung fibrosis by targeting tab1 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9901827/ https://www.ncbi.nlm.nih.gov/pubmed/36746980 http://dx.doi.org/10.1038/s41598-023-29188-6 |
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