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      Long non-coding RNA zinc finger antisense 1 expression associates with increased disease risk, elevated disease severity and higher inflammatory cytokines levels in patients with lumbar disc degeneration

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          Abstract

          This study aimed to investigate the correlation of long noncoding RNA zinc finger antisense 1 (lncRNA ZFAS1) expression with disease risk, disease severity and inflammatory cytokines levels in lumbar disc degeneration (LDD) patients.

          83 LDD patients underwent surgery and 28 traumatized, non-LDD patients underwent lumbar disc surgery (controls) were consecutively enrolled in this case-control study. Lumbar disc tissue was obtained during surgery and herniated nucleus pulposus (HNP) was isolated to detect lncRNA ZFAS1 expression and inflammatory cytokines mRNA levels by RT-qPCR, and determine protein levels of inflammatory cytokines by western blot.

          HNP lncRNA ZFAS1 expression in LDD patients was up-regulated compared with controls ( P < .001), and receiver operating characteristic (ROC) curve showed lncRNA ZFAS1 expression disclosed a good predictive value for LDD risk with area under curve (AUC) 0.753 (95% CI 0.646–0.859). And after adjustment by age, gender and body mass index (BMI), lncRNA ZFAS1 ( P = .017) remained to be an independent predictive factor for higher LDD risk. In addition, lncRNA ZFAS1 expression was positively associated with Modified Pfirrmann Grade ( P = .015). As to inflammatory cytokines, lncRNA ZFAS1 expression was observed to be positively correlated with TNF-α ( P = .002), IL-1β ( P = .007) and IL-6 ( P = .015) mRNAs expressions while reversely associated with IL-10 mRNA level ( P = .014); and lncRNA ZFAS1 expression was also positively correlated with protein levels of TNF-α ( P = .038) and IL-6 ( P = .027) while reversely associated with IL-10 protein expression ( P = .039).

          lncRNA ZFAS1 expression associates with increased risk, elevated disease severity and higher inflammatory cytokines levels in LDD patients.

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          Volatile evolution of long noncoding RNA repertoires: mechanisms and biological implications.

          Thousands of genes encoding long noncoding RNAs (lncRNAs) have been identified in all vertebrate genomes thus far examined. The list of lncRNAs partaking in arguably important biochemical, cellular, and developmental activities is steadily growing. However, it is increasingly clear that lncRNA repertoires are subject to weak functional constraint and rapid turnover during vertebrate evolution. We discuss here some of the factors that may explain this apparent paradox, including relaxed constraint on sequence to maintain lncRNA structure/function, extensive redundancy in the regulatory circuits in which lncRNAs act, as well as adaptive and non-adaptive forces such as genetic drift. We explore the molecular mechanisms promoting the birth and rapid evolution of lncRNA genes, with an emphasis on the influence of bidirectional transcription and transposable elements, two pervasive features of vertebrate genomes. Together these properties reveal a remarkably dynamic and malleable noncoding transcriptome which may represent an important source of robustness and evolvability. Copyright © 2014 Elsevier Ltd. All rights reserved.
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            LncRNA HOTAIR alleviates rheumatoid arthritis by targeting miR-138 and inactivating NF-κB pathway.

            Rheumatoid arthritis (RA) is a chronic and autoimmune-mediated inflammatory disease. We aimed to investigate the regulation of lncRNA HOTAIR in LPS-treated chondrocytes and RA mouse. Our results showed that HOTAIR expression was significantly reduced in LPS-treated chondrocytes. The HOTAIR was then over-expressed in chondrocytes by transfecting recombinant lentivirus carrying sequences encoding HOTAIR. The LPS-induced reduction of cell proliferation rate and production of two inflammatory factors interleukin (IL)-17, IL-23 were markedly inhibited. Enforced expression of HOTAIR also led to the upregulation of proliferation-related protein Ki67 and proliferating cell nuclear antigen (PCNA). Moreover, a negative correlation was detected between the expression of HOTAIR and microRNA (miR)-138, and the expression of miR-138 was significantly increased in LPS-induced chondrocytes. The effects of HOTAIR over-expression on the proliferation and inflammation were partly reversed by miR-138 overexpression. Furthermore, the overexpression of HOTAIR significantly inhibited the activation of nuclear transcription factor-κB (NF-κB) in LPS-treated chondrocytes by suppressing p65 to cell nucleus, resulting in the down-regulation of IL-1β and tumor necrosis factor (TNF)-α. In addition, the in vivo experiments exhibited that overexpression of HOTAIR increased cell proliferation and inhibited inflammation in RA rats, which were demonstrated by upregulation of Ki67 and PCNA, reduced CD4+IL-17+,CD4+IL-23+ cells, and down-regulation of p-p65, IL-1β and TNF-α. In summary, our study suggests HOTAIR plays a protective role in RA by increasing proliferation rate and inhibiting inflammation, which may be related with the regulation of miR-138 expression and NF-κB signaling pathway. These results suggest that the regulation of HOTAIR may be a promising therapeutic strategy for RA.
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              Upregulation of lncRNA HOTAIR contributes to IL-1β-induced MMP overexpression and chondrocytes apoptosis in temporomandibular joint osteoarthritis.

              Temporomandibular joint osteoarthritis (TMJ OA) is a common and heterogeneous disease that causes painful and progressive joint degeneration, which restricts daily activities, including talking and chewing. Long noncoding RNAs (lncRNAs) are an important class of genes involved in various physiological and pathological functions, including osteoarthritis (OA).The present study aimed to identify the lncRNAs that are important in TMJ OA and their potential functions. Here, we found that HOTAIR was significantly upregulated in the synovial fluid of TMJ OA patients compared with that of normal controls. Increased HOTAIR was similarly observed in the synovial fluid of TMJ OA rabbits as compared to control rabbits. Furthermore, in interleukin-1β (IL-1β)-induced TMJ OA in vitro model (primary rabbit condylar chondrocytes), the expressions of matrix metalloproteinase (MMP)-1, MMP3, MMP9 and HOTAIR were all dramatically increased. Most importantly, knockdown of HOTAIR in IL-1β-induced TMJ OA in vitro model could not only reverse the IL-1β-stimulated expressions of MMP1, MMP3 and MMP9, but also significantly decrease the apoptosis rate induced by IL-1β in primary rabbit condylar chondrocytes. Our data provides new insight into the mechanisms of chondrocytes destruction in TMJ OA.
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                December 2019
                27 December 2019
                : 98
                : 52
                : e18465
                Affiliations
                [a ]Shanghai Qeejen Bio-tech Institution, Shanghai
                [b ]General Departments, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology
                [c ]Emergency Department, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
                Author notes
                []Correspondence: Yi-Fan Wang, Emergency Department, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, No. 26 Shengli Street, Wuhan 430014 China (e-mail: yingke15929500213@ 123456163.com ); Shuang-Bing Feng, Shanghai Qeejen Bio-tech Institution, 2500 Siping Road, Shanghai 200433, China (e-mail: sbing@ 123456qeejen.com ).
                Article
                MD-D-19-06438 18465
                10.1097/MD.0000000000018465
                6946461
                31876730
                c2bc439f-5c67-4df7-9e8d-dce64062c48d
                Copyright © 2019 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc/4.0

                History
                : 14 August 2019
                : 14 October 2019
                : 19 November 2019
                Categories
                3600
                Research Article
                Observational Study
                Custom metadata
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                inflammatory cytokines,lncrna zfas1,lumbar disc degeneration,risk,severity

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