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10.1371/journal.pone.0175802 http://scihub22266oqcxt.onion/10.1371/journal.pone.0175802 C5398531!5398531 !28426699     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28426699 &cmd=llinks): Failed to open stream: HTTP request failed! 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Anti-IL-20 monoclonal antibody inhibited inflammation and protected against cartilage destruction in murine models of osteoarthritis |pdf=|usr=}}{{28426699 }} gab.com Text Anti-IL-20 monoclonal antibody inhibited inflammation and protected against cartilage destruction in murine models of osteoarthritis JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28426699 #FOAvip Osteoarthritis (OA) is a degenerative joint disease characterized by progressive destruction of articular cartilage. Interleukin (IL)-20 is a proinflammatory cytokine involved in the pathogenesis of rheumatoid arthritis. We investigated the role of IL-20 in OA and evaluated whether anti-IL-20 antibody (7E) treatment attenuates disease severity in murine models of surgery-induced OA. Immunohistochemical staining was used to detect IL-20 and its receptors expression in synovial tissue and cartilage from OA patients, and in OA synovial fibroblasts (OASFs) and chondrocytes (OACCs) from rodents with surgery-induced OA. RTQ-PCR and western blotting were used to determine IL-20-regulated OA-associated gene expression in OASFs and OACCs. OA rats and OA mice were treated with 7E. Arthritis severity was determined based on the degree of cartilage damage and the arthritis severity score. We found that IL-20 and its receptors were expressed in OASFs and OACCs. IL-20 induced TNF-?, IL-1?, MMP-1, and MMP-13 expression by activating ERK-1/2 and JNK signals in OASFs. IL-20 not only upregulated MCP-1, IL-6, MMP-1, and MMP-13 expression, but also downregulated aggrecan, type 2 collagen, TGF-?, and BMP-2 expression in OACCs. Arthritis severity was significantly lower in 7E-treated OA rats, and 7E- or MSC-treated OA mice. Therefore, we concluded that IL-20 was involved in the progression and development of OA through inducing proinflammatory cytokines and OA-associated gene expression in OASFs and OACCs. 7E reduced the severity of arthritis in murine models of surgery-induced OA. Our findings provide evidence that IL-20 is a novel target and that 7E is a potential therapeutic agent for OA. Twit Text FOAVip Anti-IL-20 monoclonal antibody inhibited inflammation and protected against cartilage destruction in murine models of osteoarthritis ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28426699 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28426699 #FOAvip English Wikipedia <ref>{{Cite pmid|28426699 }}</ref> Anti-IL-20 monoclonal antibody inhibited inflammation and protected against cartilage destruction in murine models of osteoarthritis #MMPMID28426699 Hsu YH ; Yang YY ; Huwang MH ; Weng YH ; Jou IM ; Wu PT ; Lin TY ; Wu LW ; Chang MS PLoS One 2017[]; 12 (4 ): e0175802 PMID28426699 show ga Osteoarthritis (OA) is a degenerative joint disease characterized by progressive destruction of articular cartilage. Interleukin (IL)-20 is a proinflammatory cytokine involved in the pathogenesis of rheumatoid arthritis. We investigated the role of IL-20 in OA and evaluated whether anti-IL-20 antibody (7E) treatment attenuates disease severity in murine models of surgery-induced OA. Immunohistochemical staining was used to detect IL-20 and its receptors expression in synovial tissue and cartilage from OA patients, and in OA synovial fibroblasts (OASFs) and chondrocytes (OACCs) from rodents with surgery-induced OA. RTQ-PCR and western blotting were used to determine IL-20-regulated OA-associated gene expression in OASFs and OACCs. OA rats and OA mice were treated with 7E. Arthritis severity was determined based on the degree of cartilage damage and the arthritis severity score. We found that IL-20 and its receptors were expressed in OASFs and OACCs. IL-20 induced TNF-?, IL-1?, MMP-1, and MMP-13 expression by activating ERK-1/2 and JNK signals in OASFs. IL-20 not only upregulated MCP-1, IL-6, MMP-1, and MMP-13 expression, but also downregulated aggrecan, type 2 collagen, TGF-?, and BMP-2 expression in OACCs. Arthritis severity was significantly lower in 7E-treated OA rats, and 7E- or MSC-treated OA mice. Therefore, we concluded that IL-20 was involved in the progression and development of OA through inducing proinflammatory cytokines and OA-associated gene expression in OASFs and OACCs. 7E reduced the severity of arthritis in murine models of surgery-induced OA. Our findings provide evidence that IL-20 is a novel target and that 7E is a potential therapeutic agent for OA. |*Disease Models, Animal [MESH] |Animals [MESH] |Antibodies, Monoclonal/*pharmacology [MESH] |Cartilage, Articular/metabolism/*pathology [MESH] |Cell Differentiation [MESH] |Cytokines/metabolism [MESH] |Humans [MESH] |Inflammation/metabolism/*prevention & control [MESH] |Interleukins/*immunology [MESH] |Male [MESH] |Matrix Metalloproteinase 1/metabolism [MESH] |Matrix Metalloproteinase 13/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Osteoarthritis/genetics/metabolism/*pathology [MESH] |Protein Kinases/metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH]Anti-IL-20 monoclonal antibody inhibited inflammation and protected ag(epmc).pdf DeepDyve Pubget Overpricing