Effects of sulfasalazine and tofacitinib on the protein profile of articular chondrocytes. Issue 5 (September 2014)

• Record Type: Journal Article
• Authors: Endo, Wataru; Arito, Mitsumi; Sato, Toshiyuki; Kurokawa, Manae S.; Omoteyama, Kazuki; Iizuka, Nobuko; Okamoto, Kazuki; Suematsu, Naoya; Nakamura, Hiroshi; Beppu, Moroe; Kato, Tomohiro
• Is Part Of: Modern rheumatology. Volume 24:Issue 5(2014)
• Page Start: 844
• Page End: 850
• Publication Date: 2014-09
• Subjects: Rheumatology -- Periodicals; 616.723005
• DOI: 10.3109/14397595.2013.864225
• Languages: English
• ISSNs: 1439-7595

Abstract

<abstract> <title>Abstract</title> <p> <italic>Objective.</italic> Sulfasalazine (SSZ) and tofacitinib are effective for treating rheumatoid arthritis, however, their effects on chondrocytes have not been fully understood. We here tried to elucidate their effects on chondrocyte proteins.</p> <p> <italic>Methods.</italic> We treated chondrocytes from five osteoarthritis patients with IL-1β, IL-1β+ SSZ, IL-1β+ tofacitinib, SSZ alone, and tofacitinib alone. Then, we compared protein profiles of the chondrocytes using two-dimensional differential gel electrophoresis. Further, we identified altered proteins by mass spectrometry.</p> <p> <italic>Results.</italic> Out of 892 detected protein spots, the IL-1β stimulation changed intensity of 43 spots more than 1.3-fold or less than 1/1.3-fold significantly. SSZ suppressed the IL-1β-induced intensity alteration in 16 (37%) out of the 43 protein spots. Tofacitinib suppressed the IL-1β-induced alteration in 4 (9.3%) out of the 43 spots. The production of AMP deaminase 2 and procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 were increased by IL-1β and the increase was suppressed by SSZ and by tofacitinib. SSZ alone altered intensity of 273 (31%) out of the 852 spots significantly, whereas tofacitinib alone altered intensity of only 24 (2.7%) out of them.</p> <p> <italic>Conclusion.</italic> SSZ and, to lesser extent, tofacitinib suppress the effects of IL-1β on the protein profiles of chondrocytes. Our data would promote understanding of effects of the drugs on chondrocytes.</p> </abstract>