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dc.contributor.authorWalsh, David A
dc.date.accessioned2022-05-12T12:53:47Z
dc.date.available2022-05-12T12:53:47Z
dc.date.issued2010-04
dc.identifier.citationFransès, R. E. et al. (2010) ‘Osteochondral angiogenesis and increased protease inhibitor expression in OA’, Osteoarthritis and Cartilage, 18(4), pp. 563–571en_US
dc.identifier.urihttp://hdl.handle.net/20.500.12904/15423
dc.description.abstractSummary 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
dc.description.urihttps://www.oarsijournal.com/article/S1063-4584(09)00325-2/fulltexten_US
dc.publisherOsteoarthritis and Cartilageen_US
dc.subjectTIMPen_US
dc.subjectProteaseen_US
dc.subjectAngiogenesisen_US
dc.subjectCartilageen_US
dc.subjectOsteoarthritisen_US
dc.titleOsteochondral angiogenesis and increased protease inhibitor expression in OAen_US
dc.typeArticleen_US
rioxxterms.funderDefault funderen_US
rioxxterms.identifier.projectDefault projecten_US
rioxxterms.versionNAen_US
rioxxterms.versionofrecord10.1016/j.joca.2009.11.015en_US
rioxxterms.typeJournal Article/Reviewen_US
refterms.dateFOA2022-05-12T12:53:48Z
refterms.panelUnspecifieden_US
refterms.dateFirstOnline2009-12
html.description.abstractSummary 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 cartilageen_US
rioxxterms.funder.project94a427429a5bcfef7dd04c33360d80cden_US


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