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MiR-27b-3p inhibits the progression of renal fibrosis via suppressing STAT1
Renal fibrosis is a pathologic change in chronic kidney disease (CKD). MicroRNAs (miRNAs) have been shown to play an important role in the development of renal fibrosis. However, the biological role of miR-27b-3p in renal fibrosis remains unclear. Thus, this study aimed to investigate the role of mi...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Singapore
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7900087/ https://www.ncbi.nlm.nih.gov/pubmed/33454903 http://dx.doi.org/10.1007/s13577-020-00474-z |
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author | Bai, Lin Lin, Yongtao Xie, Juan Zhang, Yiyuan Wang, Hongwu Zheng, Donghui |
author_facet | Bai, Lin Lin, Yongtao Xie, Juan Zhang, Yiyuan Wang, Hongwu Zheng, Donghui |
author_sort | Bai, Lin |
collection | PubMed |
description | Renal fibrosis is a pathologic change in chronic kidney disease (CKD). MicroRNAs (miRNAs) have been shown to play an important role in the development of renal fibrosis. However, the biological role of miR-27b-3p in renal fibrosis remains unclear. Thus, this study aimed to investigate the role of miR-27b-3p in the progression of renal fibrosis. In this study, HK-2 cells were stimulated with transforming growth factor (TGF)-β1 for mimicking fibrosis progression in vitro. The unilateral ureteric obstruction (UUO)-induced mice renal fibrosis in vivo was established as well. The results indicated that the overexpression of miR-27b-3p significantly inhibited epithelial-to-mesenchymal transition (EMT) in TGF-β1-stimulated HK-2 cells, as shown by the decreased expressions of α-SMA, collagen III, Fibronectin and Vimentin. In addition, overexpression of miR-27b-3p markedly decreased TGF-β1-induced apoptosis in HK-2 cells, as evidenced by the decreased levels of Fas, active caspase 8 and active caspase 3. Meanwhile, dual-luciferase assay showed that miR-27b-3p downregulated signal transducers and activators of transcription 1 (STAT1) expression through direct binding with the 3′-UTR of STAT1. Furthermore, overexpression of miR-27b-3p attenuated UUO-induced renal fibrosis via downregulation of STAT1, α-SMA and collagen III. In conclusion, miR-27b-3p overexpression could alleviate renal fibrosis via suppressing STAT1 in vivo and in vitro. Therefore, miR-27b-3p might be a promising therapeutic target for the treatment of renal fibrosis. |
format | Online Article Text |
id | pubmed-7900087 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Singapore |
record_format | MEDLINE/PubMed |
spelling | pubmed-79000872021-03-05 MiR-27b-3p inhibits the progression of renal fibrosis via suppressing STAT1 Bai, Lin Lin, Yongtao Xie, Juan Zhang, Yiyuan Wang, Hongwu Zheng, Donghui Hum Cell Research Article Renal fibrosis is a pathologic change in chronic kidney disease (CKD). MicroRNAs (miRNAs) have been shown to play an important role in the development of renal fibrosis. However, the biological role of miR-27b-3p in renal fibrosis remains unclear. Thus, this study aimed to investigate the role of miR-27b-3p in the progression of renal fibrosis. In this study, HK-2 cells were stimulated with transforming growth factor (TGF)-β1 for mimicking fibrosis progression in vitro. The unilateral ureteric obstruction (UUO)-induced mice renal fibrosis in vivo was established as well. The results indicated that the overexpression of miR-27b-3p significantly inhibited epithelial-to-mesenchymal transition (EMT) in TGF-β1-stimulated HK-2 cells, as shown by the decreased expressions of α-SMA, collagen III, Fibronectin and Vimentin. In addition, overexpression of miR-27b-3p markedly decreased TGF-β1-induced apoptosis in HK-2 cells, as evidenced by the decreased levels of Fas, active caspase 8 and active caspase 3. Meanwhile, dual-luciferase assay showed that miR-27b-3p downregulated signal transducers and activators of transcription 1 (STAT1) expression through direct binding with the 3′-UTR of STAT1. Furthermore, overexpression of miR-27b-3p attenuated UUO-induced renal fibrosis via downregulation of STAT1, α-SMA and collagen III. In conclusion, miR-27b-3p overexpression could alleviate renal fibrosis via suppressing STAT1 in vivo and in vitro. Therefore, miR-27b-3p might be a promising therapeutic target for the treatment of renal fibrosis. Springer Singapore 2021-01-17 2021 /pmc/articles/PMC7900087/ /pubmed/33454903 http://dx.doi.org/10.1007/s13577-020-00474-z Text en © The Author(s) 2021 Open AccessThis 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/. |
spellingShingle | Research Article Bai, Lin Lin, Yongtao Xie, Juan Zhang, Yiyuan Wang, Hongwu Zheng, Donghui MiR-27b-3p inhibits the progression of renal fibrosis via suppressing STAT1 |
title | MiR-27b-3p inhibits the progression of renal fibrosis via suppressing STAT1 |
title_full | MiR-27b-3p inhibits the progression of renal fibrosis via suppressing STAT1 |
title_fullStr | MiR-27b-3p inhibits the progression of renal fibrosis via suppressing STAT1 |
title_full_unstemmed | MiR-27b-3p inhibits the progression of renal fibrosis via suppressing STAT1 |
title_short | MiR-27b-3p inhibits the progression of renal fibrosis via suppressing STAT1 |
title_sort | mir-27b-3p inhibits the progression of renal fibrosis via suppressing stat1 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7900087/ https://www.ncbi.nlm.nih.gov/pubmed/33454903 http://dx.doi.org/10.1007/s13577-020-00474-z |
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