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Expression of the thioredoxin–thioredoxin reductase system in the inflamed joints of patients with rheumatoid arthritis

✍ Scribed by Madelon M. Maurice; Hajime Nakamura; Sonja Gringhuis; Takashi Okamoto; Shinichi Yoshida; Frank Kullmann; Sandra Lechner; Ellen A. M. Van Der Voort; Angela Leow; Johannes Versendaal; Ulf Muller-Ladner; Junji Yodoi; Paul P. Tak; Ferdinand C. Breedveld; Cornelis L. Verweij

Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
375 KB
Volume
42
Category
Article
ISSN
0004-3591

No coin nor oath required. For personal study only.

✦ Synopsis

Objective. To examine the expression of the thioredoxin (TRX)-thioredoxin reductase (TR) system in patients with rheumatoid arthritis (RA) and patients with other rheumatic diseases.

Methods. Levels of TRX in plasma and synovial fluid (SF) were measured using enzyme-linked immunosorbent assay. Cellular distribution of TRX was determined by flow cytometry and histochemistry. Cellular expression of TR was studied by in situ messenger RNA (mRNA) hybridization. The effect of oxidative stress and tumor necrosis factor ␣ (TNF␣) on TRX expression by cultured rheumatoid fibroblast-like synoviocytes was studied.

Results. Significantly increased TRX levels were found in the SF from 22 patients with RA, when compared with plasma levels in the same patients (P < 0.001) and compared with SF TRX levels in 15 patients with osteoarthritis (P < 0.001), 13 patients with gout (P < 0.05), and 9 patients with reactive arthritis (P < 0.0001). The presence of TRX could be demonstrated within the SF-derived mononuclear cells and synovial tissue (ST) of RA patients. Concordantly, expression of TR mRNA was observed in the ST of these patients. Stimulation of synovial fibroblast-like synoviocytes with either H 2 O 2 or TNF␣ induced an increase in the production of TRX.

Conclusion.

The data demonstrate significantly increased concentrations of TRX in the SF and ST of RA patients when compared with the levels in patients with other joint diseases. Evidence is presented that the local environment in the rheumatic joint contributes to increased TRX production. Based on its growthpromoting and cytokine-like properties, it is proposed that increased expression of TRX contributes to the disease activity in RA.

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