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DOI: 10.14670/HH-11-813
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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Park, Jin Sil | - |
dc.contributor.author | Kim, Sung Min | - |
dc.contributor.author | Jung, Kyung Ah | - |
dc.contributor.author | Lee, Jennifer | - |
dc.contributor.author | Kwok, Seung Ki | - |
dc.contributor.author | Cho, Mi La | - |
dc.contributor.author | Park, Sung Hwan | - |
dc.date.accessioned | 2022-02-21T10:07:06Z | - |
dc.date.available | 2022-02-21T10:07:06Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | Histology and Histopathology, Vol.32, nº5, (2017) | es |
dc.identifier.issn | 1699-5848 | - |
dc.identifier.issn | 0213-3911 | - |
dc.identifier.uri | http://hdl.handle.net/10201/117203 | - |
dc.description.abstract | Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a proinflammatory cytokine that is involved in pathogenesis of abnormal or disregulated inflammation. To verify how TWEAK/fibroblast growth factor-inducible gene 14 (Fn14) signals affect development of Th17 cells in arthritis, we utilized the SKG mouse, which spontaneously develops Th17- mediated autoimmune arthritis. Fn14-Fc was administered to zymosan A-induced arthritogenic SKG mice, and the effects in vivo were examined. Destruction of cartilage and bone damage was assessed by Hematoxylin and Eosin, and safranin O staining of the affected tissues. Phenotypic analysis of cells expressing inflammatory cytokines and angiogenesis-related factors, and the expression of transcription factor STAT3 in the affected joints were determined by immunohistochemistry. Blockade of Fn14 with Fn14-Fc reduced the clinical and histologic scores of inflammatory arthritis in the mouse model of spontaneously developed chronic autoimmune arthritis. Fn14-Fc suppressed production of inflammatory cytokines and angiogenesis-promoting factors, such as vascular endothelial growth factor and matrix metalloproteinase 3. Moreover, blocking of the TWEAK signal inhibited expression of STAT3 as well as interleukin-17 and -21 produced by Th17 cells. These results implicate TWEAK as a potential molecular target for treatment or prevention of inflammatory arthritis and autoimmune diseases such as rheumatoid arthritis. | es |
dc.format | application/pdf | es |
dc.format.extent | 10 | es |
dc.language | eng | es |
dc.publisher | Universidad de Murcia. Departamento de Biología Celular e Histología | es |
dc.relation | Sin financiación externa a la Universidad | es |
dc.rights | info:eu-repo/semantics/openAccess | es |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | TWEAK | es |
dc.subject | SKG mice | es |
dc.subject | STAT3 | es |
dc.subject | IL-17- producing T cells | es |
dc.subject | Angiogenesis | es |
dc.subject.other | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología | es |
dc.title | Inhibition of the TWEAK/Fn14 pathway attenuates autoimmune arthritis in a SKG mouse model | es |
dc.type | info:eu-repo/semantics/article | es |
dc.identifier.doi | DOI: 10.14670/HH-11-813 | - |
Aparece en las colecciones: | Vol.32, nº5 (2017) |
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Park-32-481-490-2017.pdf | 17,55 MB | Adobe PDF | Visualizar/Abrir |
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