Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 450, Issue 1, Pages 538-544Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2014.06.008
Keywords
Synoviocytes; IL-1 beta; Proteomics; TNF-independent; p62
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Funding
- National Natural and Science Foundation of China [81372135, 10972242]
- Key Clinical Program of Ministry of Health China [920100439]
- Fundamental Research Funds for the Central Universities of China [21612406]
- Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry of China
- Sun Yat-Sen University Clinical Research 5010 Program [2007050]
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IL-1 beta is readily detectable in numerous joint inflammations. It can change the transcriptomic signature of fibroblast-like synoviocytes (FLS) of arthritis toward promoting migration and invasion that are relevant to arthritis progression. We hypothesize that IL-1 beta partially contributes to the onset of osteoarthritis (OA). We compared the tissue samples from OA and fracture subjects and found that IL-1 beta expression was significantly higher in the OA synovium, while TNF-alpha expression showed no significance. We demonstrated that IL-1 beta significantly increases the IL-6 and IL-8 secretions of human normal FLS; however, IL-1 beta does not induce TNF secretion. With metabolic labeling based proteomics and pathway analysis, we found that IL-1 beta significantly increases the TNF downstream protein expression in FLS even with complete absence of TNF and/or blocking of the NF-kappa B pathway. Among these proteins, we verified that p62 can differentiate the OA from fracture synovitis. In conclusion, we demonstrated that IL-1 beta can amplify the TNF downstream protein signals in human synoviocytes in a TNF-independent manner; in addition, p62 is a potential FLS biomarker for synovitis. (C) 2014 Elsevier Inc. All rights reserved.
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