scholarly journals A critical role of Cyr61 in interleukin-17–dependent proliferation of fibroblast-like synoviocytes in rheumatoid arthritis

2009 ◽  
Vol 60 (12) ◽  
pp. 3602-3612 ◽  
Author(s):  
Qiuyu Zhang ◽  
Juanjuan Wu ◽  
Qi Cao ◽  
Lianbo Xiao ◽  
Li Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Critical Role ◽  
Interleukin 17A ◽  
Fibroblast Like Synoviocytes

scholarly journals Critical Role of Glucose Metabolism in Rheumatoid Arthritis Fibroblast-like Synoviocytes

2016 ◽  
Vol 68 (7) ◽  
pp. 1614-1626 ◽  
Author(s):  
Ricard Garcia-Carbonell ◽  
Ajit S. Divakaruni ◽  
Alessia Lodi ◽  
Ildefonso Vicente-Suarez ◽  
Arindam Saha ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Glucose Metabolism ◽  
Critical Role ◽  
Fibroblast Like Synoviocytes

Role of glucose metabolism in aggressive phenotype of fibroblast-like synoviocytes: Latest evidence and therapeutic approaches in rheumatoid arthritis

2020 ◽  
Vol 89 ◽  
pp. 107064
Author(s):  
Maryam Masoumi ◽  
Mohsen Mehrabzadeh ◽  
Salman Mahmoudzehi ◽  
Mohammad Javad Mousavi ◽  
Sirous Jamalzehi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Glucose Metabolism ◽  
Therapeutic Approaches ◽  
Aggressive Phenotype ◽  
Fibroblast Like Synoviocytes

Development of an ex vivo cellular model of rheumatoid arthritis: Critical role of cd14-positive monocyte/macrophages in the development of pannus tissue

2007 ◽  
Vol 56 (9) ◽  
pp. 2875-2885 ◽  
Author(s):  
Toshiko Nozaki ◽  
Kyoko Takahashi ◽  
Osamu Ishii ◽  
Sachio Endo ◽  
Kyoji Hioki ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Ex Vivo ◽  
Critical Role ◽  
Cellular Model ◽  
Pannus Tissue

scholarly journals The Pivotal Role of TBK1 in Inflammatory Responses Mediated by Macrophages

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Tao Yu ◽  
Young-Su Yi ◽  
Yanyan Yang ◽  
Jueun Oh ◽  
Deok Jeong ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Cell Damage ◽  
Critical Role ◽  
Biological Response ◽  
Antiviral Defense ◽  
Functional Roles ◽  
Virus Interaction

Inflammation is a complex biological response of tissues to harmful stimuli such as pathogens, cell damage, or irritants. Inflammation is considered to be a major cause of most chronic diseases, especially in more than 100 types of inflammatory diseases which include Alzheimer's disease, rheumatoid arthritis, asthma, atherosclerosis, Crohn's disease, colitis, dermatitis, hepatitis, and Parkinson's disease. Recently, an increasing number of studies have focused on inflammatory diseases. TBK1 is a serine/threonine-protein kinase which regulates antiviral defense, host-virus interaction, and immunity. It is ubiquitously expressed in mouse stomach, colon, thymus, and liver. Interestingly, high levels of active TBK1 have also been found to be associated with inflammatory diseases, indicating that TBK1 is closely related to inflammatory responses. Even though relatively few studies have addressed the functional roles of TBK1 relating to inflammation, this paper discusses some recent findings that support the critical role of TBK1 in inflammatory diseases and underlie the necessity of trials to develop useful remedies or therapeutics that target TBK1 for the treatment of inflammatory diseases.

CXCL10 and TRAIL Are Upregulated by TXNDC5 in Rheumatoid Arthritis Fibroblast-like Synoviocytes

2017 ◽  
Vol 45 (3) ◽  
pp. 335-340 ◽  
Author(s):  
Bing Xu ◽  
Jian Li ◽  
Changsun Wu ◽  
Chunyan Liu ◽  
Xinfeng Yan ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Synovial Fibroblasts ◽  
And Migration ◽  
Interfering Rna ◽  
Synovial Membranes ◽  
Necrosis Factor ◽  
Fibroblast Like Synoviocytes

Objective.Thioredoxin domain containing 5 (TXNDC5) is highly expressed in synovial membranes of rheumatoid arthritis (RA). Our study aimed to investigate the pathogenic role of TXNDC5 in RA.Methods.PCR arrays, CCK-8 assays, flow cytometry, and transwell migration assays were used to analyze cultured rheumatoid arthritis synovial fibroblasts (RASF).Results.Increased CXCL10 and tumor necrosis factor-related apoptosis-inducing ligand levels were detected in RASF transfected with anti-TXNDC5 small interfering RNA (siRNA), and decreased expression was detected in RASF transfected with TXNDC5-expressing plasmids. Significantly attenuated RASF proliferation and migration, and increased RASF apoptosis, were observed in the siRNA-transfected RASF.Conclusion.Downregulation of TXNDC5 could contribute to RASF antiangiogenic and proapoptotic features through the suppression of CXCL10 and TRAIL (tumor necrosis factor-related apoptosis-inducing ligand).

scholarly journals Dysregulation of lncRNAs in Rheumatoid Arthritis: Biomarkers, Pathogenesis and Potential Therapeutic Targets

2021 ◽  
Vol 12 ◽  
Author(s):  
Chenggui Miao ◽  
Liangliang Bai ◽  
Yaru Yang ◽  
Jinling Huang
Keyword(s):  
Rheumatoid Arthritis ◽  
Epigenetic Modification ◽  
Joint Destruction ◽  
Research Progress ◽  
Unknown Etiology ◽  
Signal Pathways ◽  
Cartilage Erosion ◽  
Chronic Autoimmune Disease ◽  
Fibroblast Like Synoviocytes

Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown etiology, mainly manifested by persistent abnormal proliferation of fibroblast-like synoviocytes (FLSs), inflammation, synovial hyperplasia and cartilage erosion, accompanied by joint swelling and joint destruction. Abnormal expression or function of long noncoding RNAs (lncRNAs) are closely related to human diseases, including cancers, mental diseases, autoimmune diseases and others. The abnormal sequence and spatial structure of lncRNAs, the disorder expression and the abnormal interaction with the binding protein will lead to the change of gene expression in the way of epigenetic modification. Increasing evidence demonstrated that lncRNAs were involved in the activation of FLSs, which played a key role in the pathogenesis of RA. In this review, the research progress of lncRNAs in the pathogenesis of RA was systematically summarized, including the role of lncRNAs in the diagnosis of RA, the regulatory mechanism of lncRNAs in the pathogenesis of RA, and the intervention role of lncRNAs in the treatment of RA. Furthermore, the activated signal pathways, the role of DNA methylation and other mechanism have also been overview in this review.

scholarly journals Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like Synoviocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Xiao-Bo Luo ◽  
Jian-Cheng Xi ◽  
Zhen Liu ◽  
Yu Long ◽  
Li-tao Li ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor Receptor ◽  
Dependent Manner ◽  
Autoimmune Inflammatory Disease ◽  
Specific Protease ◽  
Inflammatory Processes ◽  
Ubiquitin Specific Protease ◽  
Signaling Activation ◽  
Fibroblast Like Synoviocytes

Rheumatoid arthritis (RA) is a worldwide chronic autoimmune inflammatory disease which is affecting approximately 1% of the total population. It is characterized by abnormal proliferation of fibroblast-like synoviocytes (FLS) and increased production of proinflammatory cytokines. In the current study, we were aiming to investigate the role of ubiquitin-specific protease 5 (USP5) in the inflammatory process in RA-FLS. Expression of USP5 was found upregulated in RA-FLS compared with that in osteoarthritis- (OA-) FLS, and IL-1β stimulation increased USP5 expression in a time-dependent manner. Furthermore, we found that USP5 overexpression significantly aggravated proinflammatory cytokine production and related nuclear factor κB (NF-κB) signaling activation. Consistently, silencing of USP5 decreased the release of cytokines and inhibited the activation of NF-κB. In addition, USP5 was found to interact with tumor necrosis factor receptor-associated factor 6 (TRAF6) and remove its K48-linked polyubiquitination chains therefore stabilizing TRAF6. Our data showed that a USP5-positive cell regulates inflammatory processes in RA-FLS and suggested USP5 as a potential target for RA treatment.

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