Abstract
Release of FGF-2 from the pericelluar matrix of cartilage upon injury is an important early response of the tissue to injury. Even though FGF-2 knockout mice have substantially increased cartilage degradation in spontaneous and surgically induced models of osteoarthritis (OA), the in vitro literature is divided about the role of FGF-2 in articular cartilage. It is currently unclear whether FGF-2 is chondroprotective by promoting anabolic effects; or destructive through promotion of catabolic responses. One theory is that FGF-2’s opposing effects depend on which receptor it acts through. Knockout studies of FGFRs in mice have shed some light on this theory. FGFR1 conditional knockout mice are protected from developing disease while FGFR3 knockout mice have worse disease, suggesting FGFR1 mediates pro-catabolic effects and FGFR3 mediates chondroprotective effects of FGF-2. As FGFR ratios have been shown to be dysregulated in OA, we studied how receptor ratios were affected by cartilage injury, tissue culture and hypoxia.
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