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Title 

Over-expression of extracellular superoxide dismutase in mouse synovial tissue attenuates the inflammatory arthritis

Authors 

D H YuJ K YiH S YuhS J ParkH J KimK B BaeY R JiN R KimD H KimS H KimM O KimJeong Woong LeeZ Y Ryoo

Publisher 

Korean Society of Medical Biochemistry

Issue Date 

2012

Citation 

Experimental and Molecular Medicine, vol. 44, no. 9, pp. 529-535

Keywords 

ArthritisExperimentalReactive oxygen speciesRheumatoid arthritisSuperoxide dismutaseSynovial membrane --------------------------------------------------------------------------------

Abstract 

Oxidative stress such as reactive oxygen species (ROS) within the inflamed joint have been indicated as being involved as inflammatory mediators in the induction of arthritis. Correlations between extracellular- superoxide dismutase (EC-SOD) and inflammatory arthritis have been shown in several animal models of RA. However, there is a question whether the over-expression of EC-SOD on arthritic joint also could suppress the progression of disease or not. In the present study, the effect on the synovial tissue of experimental arthritis was investigated using EC-SOD over-expressing transgenic mice. The over-expression of EC- SOD in joint tissue was confirmed by RT-PCR and immunohistochemistry. The degree of the inflammation in EC-SOD transgenic mice was suppressed in the collagen-induced arthritis model. In a cytokine assay, the production of pro-inflammatory cytokines such as, IL-1β, TNFα, and matrix metalloproteinases (MMPs) was decreased in fibroblast-like synoviocyte (FLS) but not in peripheral blood. Histological examination also showed repressed cartilage destruction and bone in EC-SOD transgenic mice. In conclusion, these data suggest that the over-expression of EC-SOD in FLS contributes to the activation of FLS and protection from joint destruction by depressing the production of the pro-inflammatory cytokines and MMPs. These results provide EC-SOD transgenic mice with a useful animal model for inflammatory arthritis research.

ISSN 

1226-3613

Link 

http://dx.doi.org/10.3858/emm.2012.44.9.060

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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