MicroRNA-27a alleviates IL-1β-induced inflammatory response and articular cartilage degradation via TLR4/NF-κB signaling pathway in articular chondrocytes
Osteoarthritis (OA) is a common disease of the articular cartilage, and inflammatory response and articular cartilage degradation have been implicated in the pathogenesis of OA. In recent years, microRNAs (miRNAs) have been potentially involved in the pathogenesis of OA. However, little is known abo...
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Published in | International immunopharmacology Vol. 76; p. 105839 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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01.11.2019
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Abstract | Osteoarthritis (OA) is a common disease of the articular cartilage, and inflammatory response and articular cartilage degradation have been implicated in the pathogenesis of OA. In recent years, microRNAs (miRNAs) have been potentially involved in the pathogenesis of OA. However, little is known about the role of miRNAs in the inflammatory response and articular cartilage degradation in OA and the underlying molecular mechanism. In the present study, we analyze miRNA profiles in the articular tissues from OA patients using microarray. miR-27a has attracted considerable interest for its suppressive effects on inflammation. Subsequently, the expression levels of miR-27a were validated in the articular tissues of OA patients and IL-1β-stimulated chondrocytes. Using this IL-1β-induced chondrocyte injury model, we found that upregulation of miR-27a suppressed articular cartilage degradation, the reactive oxygen species (ROS) production and inflammatory response as reflected by reductions in pro-inflammatory cytokines, including interleukin (IL)-6 and IL-8 and tumor necrosis factor (TNF)-α. Moreover, toll-like receptor 4 (TLR4), one upstream molecule of NF-κB signaling pathway, was identified as a direct target of miR-27a in chondrocytes. Furthermore, it was demonstrated that overexpression of TLR4 by pcDNA-TLR4 markedly abrogated the inhibitory effects of miR-27a on the inflammatory response and the degeneration of articular cartilage induced by IL-1β. Our findings suggest that miR-27a may be considered as a potential therapeutic target in the treatment of OA.
•We used a miRNA microarray to analyze the miRNA profiles in normal and OA articular tissues.•MicroRNA-27a inhibits TLR4/NF-κB signaling pathway in articular chondrocytes•MicroRNA-27a alleviates IL-1β-induced inflammatory response and articular cartilage degradation in articular chondrocytes |
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AbstractList | Osteoarthritis (OA) is a common disease of the articular cartilage, and inflammatory response and articular cartilage degradation have been implicated in the pathogenesis of OA. In recent years, microRNAs (miRNAs) have been potentially involved in the pathogenesis of OA. However, little is known about the role of miRNAs in the inflammatory response and articular cartilage degradation in OA and the underlying molecular mechanism. In the present study, we analyze miRNA profiles in the articular tissues from OA patients using microarray. miR-27a has attracted considerable interest for its suppressive effects on inflammation. Subsequently, the expression levels of miR-27a were validated in the articular tissues of OA patients and IL-1β-stimulated chondrocytes. Using this IL-1β-induced chondrocyte injury model, we found that upregulation of miR-27a suppressed articular cartilage degradation, the reactive oxygen species (ROS) production and inflammatory response as reflected by reductions in pro-inflammatory cytokines, including interleukin (IL)-6 and IL-8 and tumor necrosis factor (TNF)-α. Moreover, toll-like receptor 4 (TLR4), one upstream molecule of NF-κB signaling pathway, was identified as a direct target of miR-27a in chondrocytes. Furthermore, it was demonstrated that overexpression of TLR4 by pcDNA-TLR4 markedly abrogated the inhibitory effects of miR-27a on the inflammatory response and the degeneration of articular cartilage induced by IL-1β. Our findings suggest that miR-27a may be considered as a potential therapeutic target in the treatment of OA. Osteoarthritis (OA) is a common disease of the articular cartilage, and inflammatory response and articular cartilage degradation have been implicated in the pathogenesis of OA. In recent years, microRNAs (miRNAs) have been potentially involved in the pathogenesis of OA. However, little is known about the role of miRNAs in the inflammatory response and articular cartilage degradation in OA and the underlying molecular mechanism. In the present study, we analyze miRNA profiles in the articular tissues from OA patients using microarray. miR-27a has attracted considerable interest for its suppressive effects on inflammation. Subsequently, the expression levels of miR-27a were validated in the articular tissues of OA patients and IL-1β-stimulated chondrocytes. Using this IL-1β-induced chondrocyte injury model, we found that upregulation of miR-27a suppressed articular cartilage degradation, the reactive oxygen species (ROS) production and inflammatory response as reflected by reductions in pro-inflammatory cytokines, including interleukin (IL)-6 and IL-8 and tumor necrosis factor (TNF)-α. Moreover, toll-like receptor 4 (TLR4), one upstream molecule of NF-κB signaling pathway, was identified as a direct target of miR-27a in chondrocytes. Furthermore, it was demonstrated that overexpression of TLR4 by pcDNA-TLR4 markedly abrogated the inhibitory effects of miR-27a on the inflammatory response and the degeneration of articular cartilage induced by IL-1β. Our findings suggest that miR-27a may be considered as a potential therapeutic target in the treatment of OA. •We used a miRNA microarray to analyze the miRNA profiles in normal and OA articular tissues.•MicroRNA-27a inhibits TLR4/NF-κB signaling pathway in articular chondrocytes•MicroRNA-27a alleviates IL-1β-induced inflammatory response and articular cartilage degradation in articular chondrocytes |
ArticleNumber | 105839 |
Author | Qiu, Wen-Jun Xu, Ming-Ze Zhu, Xiao-dong Ji, Yun-Han |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31520995$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1007_s12257_021_0224_9 crossref_primary_10_1016_j_cyto_2020_155397 crossref_primary_10_3389_fcell_2022_1092776 crossref_primary_10_1159_000516136 crossref_primary_10_2147_NDT_S300773 crossref_primary_10_3390_antiox13030294 crossref_primary_10_1016_j_lfs_2021_119143 crossref_primary_10_1038_s41419_020_03178_2 crossref_primary_10_1038_s41584_021_00687_y crossref_primary_10_1016_j_joca_2024_02_007 crossref_primary_10_1016_j_ecoenv_2020_111578 crossref_primary_10_1016_j_intimp_2022_108607 crossref_primary_10_1080_08923973_2022_2115924 crossref_primary_10_1186_s13018_021_02889_2 crossref_primary_10_1186_s12974_020_02040_8 crossref_primary_10_1016_j_lfs_2023_122272 crossref_primary_10_1186_s12969_023_00833_8 crossref_primary_10_3389_fcell_2021_774370 crossref_primary_10_3390_life12111914 crossref_primary_10_1016_j_ebiom_2021_103283 |
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Keywords | MicroRNA-27a TLR4/NF-κB signaling pathway Inflammatory response Articular cartilage degradation Osteoarthritis |
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Snippet | Osteoarthritis (OA) is a common disease of the articular cartilage, and inflammatory response and articular cartilage degradation have been implicated in the... |
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SubjectTerms | Aged Articular cartilage degradation Biomedical materials Cartilage Cartilage (articular) Cartilage diseases Cartilage, Articular - immunology Cells, Cultured Chondrocytes Chondrocytes - immunology Cytokines Degeneration Degradation Humans IL-1β Inflammation Inflammation - immunology Inflammatory response Interleukin 8 Interleukin-1beta - immunology MicroRNA-27a MicroRNAs MicroRNAs - immunology Middle Aged miRNA NF-kappa B - immunology NF-κB protein Osteoarthritis Osteoarthritis - immunology Pathogenesis Reactive oxygen species Reactive Oxygen Species - immunology Ribonucleic acid RNA Signal Transduction Signaling Target recognition Therapeutic applications TLR4 protein TLR4/NF-κB signaling pathway Toll-Like Receptor 4 - immunology Toll-like receptors Tumor necrosis factor-TNF Tumor necrosis factor-α |
Title | MicroRNA-27a alleviates IL-1β-induced inflammatory response and articular cartilage degradation via TLR4/NF-κB signaling pathway in articular chondrocytes |
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