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miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis
miR-410-3p acts as an oncogene or a tumor suppressor in some malignancies. However, its role in rheumatoid arthritis (RA) is unknown. The study was conducted to investigate the effect of miR-410-3p on the pathogenesis of RA. Real-time RT-PCR was used to determine the mRNA levels of miR-410-3p in syn...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6394566/ https://www.ncbi.nlm.nih.gov/pubmed/30242542 http://dx.doi.org/10.1007/s10753-018-0896-2 |
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author | Wang, YueJiao Xu, NeiLi Zhao, Shuai Jiao, Ting Fu, WenYi Yang, LiLi Zhang, Ning |
author_facet | Wang, YueJiao Xu, NeiLi Zhao, Shuai Jiao, Ting Fu, WenYi Yang, LiLi Zhang, Ning |
author_sort | Wang, YueJiao |
collection | PubMed |
description | miR-410-3p acts as an oncogene or a tumor suppressor in some malignancies. However, its role in rheumatoid arthritis (RA) is unknown. The study was conducted to investigate the effect of miR-410-3p on the pathogenesis of RA. Real-time RT-PCR was used to determine the mRNA levels of miR-410-3p in synovial tissues and fibroblast-like synoviocytes (FLSs). An ELISA was performed to examine the production levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and matrix metalloproteinase (MMP)-9. Western blotting was conducted to determine the protein levels of IκB-α, p-IκBα, p65, and p-p65. Nuclear factor (NF)-κB activation and nuclear translocation assays were performed to confirm the activation of NF-κB. We found that the expression level of miR-410-3p was downregulated in synovial tissues and FLSs from RA. Overexpression of miR-410-3p significantly reduced the secretion of TNF-α, IL-1β, IL-6, and MMP-9 in human RA fibroblast-like synoviocytes (HFLS-RA); whereas miR-410-3p inhibition increased the expression levels of these cytokines. Furthermore, miR-410-3p suppresses the activation of NF-κB signaling pathway. Moreover, NF-κB inhibitor restored the elevation of TNF-α, IL-1β, IL-6, and MMP-9 induced by miR-410-3p inhibition. Our results demonstrate that miR-410-3p acts an inflammatory suppressor in the pathogenesis of RA by regulating the NF-κB signaling pathway. These data suggest a novel function of miR-410-3p and provide insight into the complex mechanisms involved in RA. |
format | Online Article Text |
id | pubmed-6394566 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-63945662019-03-15 miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis Wang, YueJiao Xu, NeiLi Zhao, Shuai Jiao, Ting Fu, WenYi Yang, LiLi Zhang, Ning Inflammation Original Article miR-410-3p acts as an oncogene or a tumor suppressor in some malignancies. However, its role in rheumatoid arthritis (RA) is unknown. The study was conducted to investigate the effect of miR-410-3p on the pathogenesis of RA. Real-time RT-PCR was used to determine the mRNA levels of miR-410-3p in synovial tissues and fibroblast-like synoviocytes (FLSs). An ELISA was performed to examine the production levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and matrix metalloproteinase (MMP)-9. Western blotting was conducted to determine the protein levels of IκB-α, p-IκBα, p65, and p-p65. Nuclear factor (NF)-κB activation and nuclear translocation assays were performed to confirm the activation of NF-κB. We found that the expression level of miR-410-3p was downregulated in synovial tissues and FLSs from RA. Overexpression of miR-410-3p significantly reduced the secretion of TNF-α, IL-1β, IL-6, and MMP-9 in human RA fibroblast-like synoviocytes (HFLS-RA); whereas miR-410-3p inhibition increased the expression levels of these cytokines. Furthermore, miR-410-3p suppresses the activation of NF-κB signaling pathway. Moreover, NF-κB inhibitor restored the elevation of TNF-α, IL-1β, IL-6, and MMP-9 induced by miR-410-3p inhibition. Our results demonstrate that miR-410-3p acts an inflammatory suppressor in the pathogenesis of RA by regulating the NF-κB signaling pathway. These data suggest a novel function of miR-410-3p and provide insight into the complex mechanisms involved in RA. Springer US 2018-09-21 2019 /pmc/articles/PMC6394566/ /pubmed/30242542 http://dx.doi.org/10.1007/s10753-018-0896-2 Text en © The Author(s) 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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. |
spellingShingle | Original Article Wang, YueJiao Xu, NeiLi Zhao, Shuai Jiao, Ting Fu, WenYi Yang, LiLi Zhang, Ning miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis |
title | miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis |
title_full | miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis |
title_fullStr | miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis |
title_full_unstemmed | miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis |
title_short | miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis |
title_sort | mir-410-3p suppresses cytokine release from fibroblast-like synoviocytes by regulating nf-κb signaling in rheumatoid arthritis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6394566/ https://www.ncbi.nlm.nih.gov/pubmed/30242542 http://dx.doi.org/10.1007/s10753-018-0896-2 |
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