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Proteomic changes in articular cartilage of human endemic osteoarthritis in China
Author(s) -
Ma WeiJuan,
Guo Xiong,
Liu JiangTao,
Liu RuiYu,
Hu JianWen,
Sun AnGuo,
Yu YueXiang,
Lammi Mikko J.
Publication year - 2011
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.201000636
Subject(s) - cytoskeleton , pathogenesis , cartilage , cofilin , biology , chondrocyte , heat shock protein , difference gel electrophoresis , proteomics , peroxiredoxin , osteoarthritis , microbiology and biotechnology , actin cytoskeleton , pathology , cell , medicine , immunology , biochemistry , gene , anatomy , peroxidase , enzyme , alternative medicine
Kashin–Beck disease (KBD) is a chronic endemic osteochondropathy with unclear pathogenesis. It is a degenerative disease similar to osteoarthritis, but with different manifestations of cartilage damage. The aim of this investigation was to show the protein changes in KBD cartilage and to identify the candidate proteins in order to understand the pathogenesis of the disease. Proteins were extracted from the media of primary cell cultures of KBD and normal chondrocytes, and separated by two‐dimensional fluorescence difference gel electrophoresis (2‐D DIGE). MALDI‐TOF/TOF analysis revealed statistically significant differences in 27 proteins from KBD chondrocyte cultures, which consisted of 17 up‐regulated and ten down‐regulated proteins. The results were further validated by Western blot analysis. The proteins identified are mainly involved in cellular redox homeostasis and stress response (MnSOD, Hsp27, Peroxiredoxin‐1, and Cofilin‐1), glycolysis (PGK‐1, PGM‐1, α‐enolase), and cell motility and cytoskeletal organization (Actin, Calponin‐2, and Keratin). These KBD‐associated proteins indicate that cytoskeletal remodeling, glycometabolism, and oxidative stress are abnormal in KBD articular cartilage.