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      N 6-methyladenosine (m 6A) methyltransferase METTL3-mediated LINC00680 accelerates osteoarthritis through m 6A/SIRT1 manner

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          Abstract

          Increasing evidence suggest the biological roles of N 6-methyladenosine (m 6A) and long noncoding RNAs (lncRNAs) in the bone disease, especially osteoarthritis (OA). However, the interaction of m 6A and lncRNA in osteoarthritis is still unclear. Here, we found that a m 6A-related lncRNA LINC00680 upregulated in the OA tissue and IL-1β-induced isolated primary chondrocytes. Functionally, in IL-1β-induced chondrocytes, silencing of LINC00680 recovered the proliferation and repressed the extracellular matrix (ECM) degradation. Mechanistically, m 6A methyltransferase METTL3 combined tithe the m 6A site of LINC00680 to up-regulate its expression. Moreover, LINC00680 interacted with SIRT1 mRNA through binding at m 6A site on SIRT1 mRNA 3′-UTR, thereby enhancing the stability of SIRT1 mRNA. Overall, these findings exhibited a role of LINC00680/m 6A/SIRT1 mRNA complex in chondrocytes. Taken together, the present study intends to uncover the mechanism by which METTL3-mediated LINC00680 accelerates OA progression, which may provide novel insight for OA.

          Abstract

          LINC00680/m6A/IGF2BP2/SIRT1 axis promotes the OA progression in chondrocyte.

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          Most cited references32

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          RNA N 6 -methyladenosine modification in cancers: current status and perspectives

          Xiaolan Deng, Rui Su, Hengyou Weng … (2018)
          N 6-methyladenosine (m6A), the most abundant internal modification in eukaryotic messenger RNAs (mRNAs), has been shown to play critical roles in various normal bioprocesses such as tissue development, stem cell self-renewal and differentiation, heat shock or DNA damage response, and maternal-to-zygotic transition. The m6A modification is deposited by the m6A methyltransferase complex (MTC; i.e., writer) composed of METTL3, METTL14 and WTAP, and probably also VIRMA and RBM15, and can be removed by m6A demethylases (i.e., erasers) such as FTO and ALKBH5. The fates of m6A-modified mRNAs rely on the functions of distinct proteins that recognize them (i.e., readers), which may affect the stability, splicing, and/or translation of target mRNAs. Given the functional importance of the m6A modification machinery in normal bioprocesses, it is not surprising that evidence is emerging that dysregulation of m6A modification and the associated proteins also contributes to the initiation, progression, and drug response of cancers. In this review, we focus on recent advances in the study of biological functions and the underlying molecular mechanisms of dysregulated m6A modification and the associated machinery in the pathogenesis and drug response of various types of cancers. In addition, we also discuss possible therapeutic interventions against the dysregulated m6A machinery to treat cancers.
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            Matrix metalloproteinases: role in arthritis.

            Peter S Burrage, Kimberlee S Mix, Constance Brinckerhoff (2006)
            The irreversible destruction of the cartilage, tendon, and bone that comprise synovial joints is the hallmark of both rheumatoid arthritis (RA) and osteoarthritis (OA). While cartilage is made up of proteoglycans and type II collagen, tendon and bone are composed primarily of type I collagen. RA is an autoimmune disease afflicting numerous joints throughout the body; in contrast, OA develops in a small number of joints, usually resulting from chronic overuse or injury. In both diseases, inflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) stimulate the production of matrix metalloproteinases (MMPs), enzymes that can degrade all components of the extracellular matrix. The collagenases, MMP-1 and MMP-13, have predominant roles in RA and OA because they are rate limiting in the process of collagen degradation. MMP-1 is produced primarily by the synovial cells that line the joints, and MMP-13 is a product of the chondrocytes that reside in the cartilage. In addition to collagen, MMP-13 also degrades the proteoglycan molecule, aggrecan, giving it a dual role in matrix destruction. Expression of other MMPs such as MMP-2, MMP-3 and MMP-9, is also elevated in arthritis and these enzymes degrade non-collagen matrix components of the joints. Significant effort has been expended in attempts to design effective inhibitors of MMP activity and/or synthesis with the goal of curbing connective tissues destruction within the joints. To date, however, no effective clinical inhibitors exist. Increasing our knowledge of the crystal structures of these enzymes and of the signal transduction pathways and molecular mechanisms that control MMP gene expression may provide new opportunities for the development of therapeutics to prevent the joint destruction seen in arthritis.
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              Osteoarthritis

              Benjamin Abramoff, Franklin E. Caldera (2019)
              Osteoarthritis (OA) is a worldwide endemic and debilitating disease. Previously thought to simply be damaged from "wear and tear," OA is now understood to be a complex interaction of local and systemic factors. This article reviews the pathology, symptoms, diagnosis, and various conservative, surgical, and novel treatments of OA.
              Article 0 comments Cited 300 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Guangxin Huang:
                ORCID: http://orcid.org/0000-0002-1277-9141
                huangguang06@smu.edu.cn
                Journal
                Journal ID (nlm-ta): Cell Death Discov
                Journal ID (iso-abbrev): Cell Death Discov
                Title: Cell Death Discovery
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2058-7716
                Publication date (Electronic): 2 May 2022
                Publication date PMC-release: 2 May 2022
                Publication date Collection: 2022
                Volume: 8
                Electronic Location Identifier: 240
                Affiliations
                [1 ]GRID grid.413107.0, Department of Joint Surgery, , Center for Orthopaedics Surgery, The Third Affiliated Hospital of Southern Medical University (Academy of Orthopaedics Guangdong Province), ; Tianhe District, Guangzhou, Guangdong Province China
                [2 ]Orthopaedics Hospital of Guangdong Province, Tianhe District, Guangzhou, Guangdong Province China
                [3 ]GRID grid.412631.3, Department of Orthopaedics, , First Affiliated Hospital of Xinjiang Medical University, ; Urumqi, Xinjiang China
                [4 ]GRID grid.459690.7, Karamay Central Hospital, ; Karamay, Xinjiang China
                Author information
                http://orcid.org/0000-0002-1277-9141
                Article
                Publisher ID: 890
                DOI: 10.1038/s41420-022-00890-0
                PMC ID: 9061755
                PubMed ID: 35501316
                SO-VID: 8d7fe8a1-2597-44ce-840f-1f4161a9c744
                Copyright © © The Author(s) 2022
                License:

                Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 6 November 2021
                Date revision received : 20 December 2021
                Date accepted : 25 January 2022
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2022

                Keywords: long non-coding rnas,osteoarthritis
                Data availability:
                Keywords: long non-coding rnas, osteoarthritis

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