Long Non-Coding RNA RASSF8-AS1 Promotes M1 Macrophage Polarization in Osteoarthritis via Moderating miR-27a-3p
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- Shi Haijun
- The First People’s Hospital of Aksu Prefecture
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- Liu Meizhi
- Department of Rheumatology, Hebei General Hospital
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- Ma Wenhan
- Department of Cardiology, the Second Hospital of Shandong University
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- Chen Zhigang
- Department of Orthopedic Surgery, The First Affiliated Hospital of Xi’an Medical University
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- Shi Yongyun
- Department of 1<sup>st</sup> Orthopedic Surgery, Nanjing Luhe People’s Hospital
書誌事項
- 公開日
- 2025
- 資源種別
- journal article
- DOI
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- 10.1620/tjem.2024.j092
- 公開者
- 東北ジャーナル刊行会
この論文をさがす
説明
<p>Long non-coding RNAs are major regulators in the pathophysiology of osteoarthritis (OA), which involves the dysfunction of cartilage and synovium. The aim of this study was, therefore, to discover the role of RASSF8-AS1 in cartilage degradation and M1 macrophage polarization during OA. Healthy and OA cartilage and synovium were collected. After measuring RASSF8-AS1 levels in tissues and lipopolysaccharide (LPS)- or IL-1β-induced cells, the role of RASSF8-AS1 in the expression of cartilage degradation markers and M1 macrophage molecules was assessed in vitro. The apoptotic rate of IL-1β-stimulated chondrocytes, with or without RASSF8-AS1 overexpression, was quantified using flow cytometry. RASSF8-AS1 was significantly upregulated not only in cartilage and synovium from OA patients, but also in IL-1β- or LPS-induced cells, compared to normal controls. A decrease in RASSF8-AS1 level increased the expression of chondrogenic markers, but reduced the expression of genes encoding matrix-degrading proteases, thereby reducing cell apoptosis. Downregulation of RASSF8-AS1 reduced the M1 macrophage markers in RAW264.7 cells and bone marrow-derived macrophages. RASSF8-AS1 may be a ceRNA for miR-27a-3p. These findings support the role of RASSF8-AS1 as a promoting factor of cartilage degradation and M1 macrophage polarization in OA.</p>
収録刊行物
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- The Tohoku Journal of Experimental Medicine
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The Tohoku Journal of Experimental Medicine 266 (3), 219-227, 2025
東北ジャーナル刊行会
