Journal
BIOMEDICAL RESEARCH-TOKYO
Volume 32, Issue 3, Pages 209-215Publisher
BIOMEDICAL RESEARCH PRESS LTD
DOI: 10.2220/biomedres.32.209
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- Chugai Pharmaceutical Company
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Increased fibronectin fragments are thought to contribute to joint destruction in osteoarthritis (OA). However, the mechanism whereby fibronectin fragments cause catabolic activities is not totally understood. While COOH-terminal heparin-binding fibronectin fragment (HBFN-f) has been shown to activate nuclear factor (NF)-kappa B pathway, intracellular upstream events that cause NF-kappa B up-regulation in response to HBFN-f remain unclear. Thus, this study was aimed to elucidate the involvement of phosphoinositide-3-OH kinase (PI3K)/Akt pathway in NF-kappa B activation by HBFN-f in OA chondrocytes. In chondrocyte monolayer cultures, HBFN-f stimulated nitric oxide (NO) production in association with phosphorylation of NF-kappa B and Akt. Inhibition studies using LY294002 revealed the requirement of PI3K/Akt pathway for NO production and NF-kappa B activation by HBFN-f. Anti-CD44 treatment with anti-CD44 antibody and hyaluronan resulted in significant inhibition of HBFN-f actions on NO, NF-kappa B, and Akt. Herein, we provided the first evidence that HBFN-f activates PI3K/Akt pathway leading to up-regulation of NF-kappa B through interaction with CD44.
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