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      LncRNA MIR4435-2HG is downregulated in osteoarthritis and regulates chondrocyte cell proliferation and apoptosis

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          Abstract

          Purpose

          MIR4435-2HG is an oncogenic lncRNA in gastric cancer and lung cancer. Our preliminary microarray data showed that MIR4435-2HG was downregulated in osteoarthritis plasma specimen, indicating the possible involvement of MIR4435-2HG in osteoarthritis.

          Results

          MIR4435-2HG was downregulated in plasma of osteoarthritis than in plasma of healthy controls. Reduced levels of MIR4435-2HG expression effectively distinguished osteoarthritis patients from the control group. Expression levels of MIR4435-2HG increased after treatment. Overexpression of MIR4435-2HG promoted, while MIR4435-2HG knockdown inhibited the proliferation of chondrocytes. In contrast, MIR4435-2HG overexpression inhibited, while MIR4435-2HG knockdown promoted the apoptosis of chondrocytes.

          Conclusion

          MIR4435-2HG is downregulated in osteoarthritis and regulates chondrocyte cell proliferation and apoptosis.

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          Characterization of articular cartilage and subchondral bone changes in the rat anterior cruciate ligament transection and meniscectomized models of osteoarthritis.

          Tadashi Hayami, Maureen Pickarski, Ya Zhuo … (2006)
          Osteoarthritis (OA) is a chronic joint disease characterized by cartilage destruction, subchondral bone sclerosis, and osteophyte formation. Subchondral bone stiffness has been proposed to initiate and/or contribute to cartilage deterioration in OA. The purpose of this study was to characterize subchondral bone remodeling, cartilage damage, and osteophytosis during the disease progression in two models of surgically induced OA. Rat knee joints were subjected either to anterior cruciate ligament transection (ACLT) alone or in combination with resection of medial menisci (ACLT + MMx). Histopathological changes in the surgical joints were compared with sham at 1, 2, 4, 6, and 10 weeks post-surgery. Using a modified Mankin scoring system, we demonstrate that articular cartilage damage occurs within 2 weeks post-surgery in both surgical models. Detectable cartilage surface damage and proteoglycan loss were observed as early as 1 week post-surgery. These were followed by the increases in vascular invasion into cartilage, in loss of chondrocyte number and in cell clustering. Histomorphometric analysis revealed subchondral bone loss in both models within 2 weeks post-surgery followed by significant increases in subchondral bone volume relative to sham up to 10 weeks post-surgery. Incidence of osteophyte formation was optimally observed in ACLT joints at 10 weeks and in ACLT + MMx joints at 6 weeks post-surgery. In summary, the two surgically induced rat OA models share many characteristics seen in human and other animal models of OA, including progressive articular cartilage degradation, subchondral bone sclerosis, and osteophyte formation. Moreover, increased subchondral bone resorption is associated with early development of cartilage lesions, which precedes significant cartilage thinning and subchondral bone sclerosis. Together, these findings support a role for bone remodeling in OA pathogenesis and suggest that these rat models are suitable for evaluating bone resorption inhibitors as potential disease-modifying pharmaco-therapies.
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            Chondrocyte death by apoptosis is associated with cartilage matrix degradation.

            C Fuller, C Thomas, Munir M. Sharif … (2006)
            To investigate the frequency of chondrocyte apoptosis in equine articular cartilage (AC) specimens and to examine the relationship between the process of cell death and the degree of cartilage degradation using a direct quantification of numbers of apoptotic cells and expression of active caspase-3. AC from equine metacarpophalangeal (MCP), proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints was used and each joint was graded macroscopically for cartilage degradation (macroscopic osteoarthritis (OA) score). Cartilage sections were graded using a 'modified' Mankin scoring system. Apoptosis of chondrocytes in cartilage sections was assessed morphologically by appearance of apoptotic features (direct method) and by expression of active caspase-3 using indirect immunohistochemistry. The extent of apoptosis assessed by the direct method did not show any relationship with increasing severity of OA (P=0.72). However, there was a significant positive correlation between 'modified' Mankin score and apoptosis determined by caspase-3, with the extent of apoptosis found to increase linearly with increasing severity of OA (r=0.44, P=0.0043). Caspase-3 expression was found to be significantly higher in the superficial and middle zones than in the deep zone (P<0.001). In the superficial, middle and deep zones, expression of caspase-3 was significantly higher in the MCP joint than in the PIP joint (P=0.013, P=0.0018 and P=0.029, respectively). Within the MCP joints, apoptosis was higher in the lateral compartment compared to the medial (P=0.053). The data presented in this study demonstrate that chondrocyte apoptosis is positively associated with degree of cartilage matrix damage and that the extent of apoptosis varies with cartilage zones and mechanical loading environment of the joint.
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              Identification of long noncoding RNA associated with osteoarthritis in humans.

              Dan Xing, Jin-qian Liang, Yan. Li … (2014)
              Long noncoding RNAs (lncRNAs) are an important class of genes involved in various biological functions; however, knowledge about lncRNAs in osteoarthritis (OA) is limited. Therefore, the present study aimed to identify which lncRNAs are expressed in OA versus normal cartilage.
              Article 0 comments Cited 70 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yu Xiao:
                ORCID: http://orcid.org/0000-0001-9964-5703
                omammeaz715196438@126.com
                Yucheng Bao: pqnohzq282231631@126.com
                Liang Tang: ekfadocq12077@126.com
                Li Wang: tatyeuri431842@126.com
                Journal
                Journal ID (nlm-ta): J Orthop Surg Res
                Journal ID (iso-abbrev): J Orthop Surg Res
                Title: Journal of Orthopaedic Surgery and Research
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1749-799X
                Publication date (Electronic): 6 August 2019
                Publication date PMC-release: 6 August 2019
                Publication date Collection: 2019
                Volume: 14
                Electronic Location Identifier: 247
                Affiliations
                [1 ]ISNI 0000 0004 1799 2608, GRID grid.417028.8, Department of Orthopaedic Surgery, , Tianjin Hospital, ; No.406 Jiefang South Road, Hexi, Tianjin City, 300211 People’s Republic of China
                [2 ]GRID grid.417026.6, Department of Orthopaedic Surgery, , Tianjin Haihe Hospital, ; 890 Jingu Road, Shuanggang Zhen, Jinnan, Tianjin, 300350 People’s Republic of China
                Author information
                http://orcid.org/0000-0001-9964-5703
                Article
                Publisher ID: 1278
                DOI: 10.1186/s13018-019-1278-7
                PMC ID: 6683450
                PubMed ID: 31387631
                SO-VID: 946416d3-8636-4eb7-b32d-52ba632c6a20
                Copyright © © The Author(s). 2019
                License:

                Open AccessThis 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. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 22 March 2019
                Date accepted : 11 July 2019
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Surgery
                Keywords: osteoarthritis,lncrna mir4435-2hg,proliferation,apoptosis
                Data availability:
                ScienceOpen disciplines: Surgery
                Keywords: osteoarthritis, lncrna mir4435-2hg, proliferation, apoptosis

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