Objective: Evaluation of the role of VEGF in cartilage pathophysiology. Methods: VEGF release from chondrocytes in the presence of IL-1β, TGFβ and IL-10 was detected by immunoassay. VEGF receptor -1 and -2 expression and VEGF ability to modulate caspase-3 and cathepsin B expression were detected by immunohistochemistry on cartilage biopsies and cartilage explants. VEGF effects on chondrocyte proliferation was analysed by a fluorescent dye that binds nucleic acids. Results: VEGF production by osteoartritis (OA) chondrocytes was significantly reduced by IL-10 while it was increased in the presence of TGFβ. Cartilage VEGFR-1 immunostaining was significantly downregulated in 'early' OA patients compared to normal controls (NC). VEGFR-2 expression was negligible both in OA and in NC. VEGF decreased the expression of caspase-3 and cathepsin B, whereas it did not affect proliferation. Conclusion: VEGF is able to down-modulate chrondrocyte activities related to catabolic events involved in OA cartilage degradation.
|Number of pages||7|
|Journal||Clinical and Experimental Rheumatology|
|Publication status||Published - Jul 2005|
- Vascular endothelial growth factor
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