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Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1.
- Source :
-
Scientific reports [Sci Rep] 2023 Feb 06; Vol. 13 (1), pp. 2128. Date of Electronic Publication: 2023 Feb 06. - Publication Year :
- 2023
-
Abstract
- 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.<br /> (© 2023. The Author(s).)
- Subjects :
- Humans
Mice
Animals
Lung pathology
Fibrosis
Bleomycin toxicity
Bleomycin metabolism
Fibroblasts metabolism
Transforming Growth Factor beta metabolism
Transforming Growth Factor beta1 metabolism
Adaptor Proteins, Signal Transducing genetics
Adaptor Proteins, Signal Transducing metabolism
MicroRNAs metabolism
Idiopathic Pulmonary Fibrosis chemically induced
Idiopathic Pulmonary Fibrosis genetics
Idiopathic Pulmonary Fibrosis metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 2045-2322
- Volume :
- 13
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Scientific reports
- Publication Type :
- Academic Journal
- Accession number :
- 36746980
- Full Text :
- https://doi.org/10.1038/s41598-023-29188-6