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Serum proteome analysis in patients with rheumatoid arthritis receiving therapy with etanercept, a chimeric tumor necrosis factor‐alpha receptor
Author(s) -
Yanagida Mitsuaki,
Jung Giman,
Tanaka Yoshinori,
Sone Saburo,
Fujishiro Maki,
Ikeda Keigo,
Nozawa Kazuhisa,
Kaneko Hiroshi,
Takasaki Yoshinari,
Ogawa Hideoki,
Takamori Kenji,
Sekigawa Iwao
Publication year - 2012
Publication title -
international journal of rheumatic diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 41
eISSN - 1756-185X
pISSN - 1756-1841
DOI - 10.1111/j.1756-185x.2012.01816.x
Subject(s) - etanercept , medicine , rheumatoid arthritis , tumor necrosis factor alpha , cartilage , pathogenesis , arthritis , proteome , immunology , cancer research , bioinformatics , biology , anatomy
Aim Rheumatoid arthritis ( RA ) is a chronic inflammatory disorder of the synovium resulting in the destruction of affected joint cartilage and bone structures. Etanercept is a biological agent that blocks the tumor necrosis factor‐α ( TNF ‐α)‐mediated inflammatory processes in RA patients, and has a regenerative effect on cartilage. In order to identify novel disease‐related proteins and candidate biomarkers, we performed proteomic profiling of the serum in patients with RA who were treated with etanercept. Method Serum samples were obtained from eight RA patients before and after etanercept treatment. The low molecular weight proteins in the serum were concentrated and analyzed by liquid chromatography‐tandem mass spectrometry. The results before and after etanercept treatment were compared by the spectrum count method. Results Among a total of 477 proteins identified, 12 were found to be decreased and five were increased by etanercept treatment. Some of the changed proteins were known to be related to RA , and most of the other changed proteins may play possible roles in the TNF ‐α signaling pathway or the state of cartilage and extracellular matrix. Conclusion The present proteomic study identified several proteins that could be involved in the pathogenesis of RA . These findings could thus lead to the identification of novel candidate disease‐related protein biomarkers for RA , or indicate new targets for therapy.