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    Osteochondral angiogenesis and increased protease inhibitor expression in OA

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    Author
    Walsh, David A
    Keyword
    TIMP
    Protease
    Angiogenesis
    Cartilage
    Osteoarthritis
    Date
    2010-04
    
    Metadata
    Show full item record
    Publisher's URL
    https://www.oarsijournal.com/article/S1063-4584(09)00325-2/fulltext
    Abstract
    Summary Objective Normal cartilage is resistant to vascular invasion and anti-angiogenic protease inhibitors may contribute to its avascular status. We hypothesized that dysregulated expression of four key anti-angiogenic protease inhibitors may contribute to increased osteochondral vascularity in osteoarthritis (OA). Results All protease inhibitors and VEGF were localised to chondrocytes near the articular surface, less often in the middle zone, and rarely to deep chondrocytes. Scores for VEGF, TIMP-1, TIMP-3, SLPI and PAI-1 were all increased in OA compared with PM, and higher scores were associated with greater chondropathy. Chondrocyte expression of VEGF was associated with higher osteochondral vascular density (r=0.32, P<0.05), whereas protease inhibitors were not. Conclusions The resistance of normal articular cartilage to vascular invasion may be more due to its matrix environment than ongoing protease inhibitor expression. Upregulation of protease inhibitors by superficial chondrocytes in OA may moderate the angiogenic effects of growth factors such as VEGF. However, failure of deep chondrocytes to express anti-angiogenic protease inhibitors may permit vascular invasion into the articular cartilage
    Citation
    Fransès, R. E. et al. (2010) ‘Osteochondral angiogenesis and increased protease inhibitor expression in OA’, Osteoarthritis and Cartilage, 18(4), pp. 563–571
    Publisher
    Osteoarthritis and Cartilage
    Type
    Article
    URI
    http://hdl.handle.net/20.500.12904/15423
    Collections
    Rheumatology

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