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Proteomic analysis of hyaluronate‐regulated proteins involved in chondroprotective effect under oxidative stress (LB177)
Author(s) -
Yu ChiaJung,
Ko ChunJung,
Hsieh ChangHsun,
Chien ChiangTing,
Huang LienHung,
Lee ChienWei,
Jiang ChingChuan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb177
Subject(s) - oxidative stress , hyaluronic acid , osteoarthritis , chemistry , apoptosis , blot , cartilage , proteomics , superoxide , programmed cell death , cell , microbiology and biotechnology , biochemistry , medicine , biology , pathology , gene , anatomy , enzyme , alternative medicine
Osteoarthritis (OA), the most common type of arthritis, is a degenerative joint disease. Oxidative stress is well known to play important roles in cartilage degradation and pathogenesis of OA. The intra‐articular injection of hyaluronic acid (IAHA) is accepted as an effective clinical therapy for OA, but we do not yet fully understand the mechanisms underlying the effects of HA on OA chondrocytes under oxidative stress. Here, we show for the first time that IAHA significantly reduces the synovial fluid levels of hydrogen peroxide (H 2 O 2 ) and superoxide (O 2 − ) in patients with knee OA. We also demonstrate that HA suppresses H 2 O 2 ‐induced cell death in human OA chondrocytes. Proteomic approaches (2‐DE combined with mass spectrometry) allowed us to identify 13 protein spots corresponding to 12 non‐redundant proteins as HA‐regulated proteins in OA chondrocytes under oxidative stress. The expression levels of three putative HA‐regulated proteins (TALDO, ANXA1 and EF2) in control, H 2 O 2 ‐, HA‐ and HA/H 2 O 2 ‐treated OA chondrocytes were verified by Western blotting and the results indeed support the notion that HA acts in anti‐oxidation, anti‐apoptosis, and the promotion of cell survival. Our results collectively demonstrate the utility of proteomic approaches and provide new insights into the chondroprotective effects of HA on OA. Grant Funding Source : Supported by National Science Council, R.O.C.