Journal of Oral Tissue Engineering
Fibronectin Inhibited RANKL-induced Differentiation into Osteoclast
Seiji GODA1, Hiroshi HAYASHI2, Yosuke UJII2, Osamu TAKEUCHI3, Reiko KOMASA3, Eisuke DOMAE1, Kazuyo YAMAMOTO3, Naoyuki MATSUMOTO2 and Takashi IKEO1
1Department of Biochemistry, 2Department of Orthodontics,
3Department of Operative Dentistry,
Osaka Dental University, Osaka, Japan
J Oral Tissue Engin 2014;11(3):227-233
Bone remodeling is required for orthodontic tooth movement, and it is essential to clarify the mechanisms. In bone remodeling mechanism, the differentiation into osteoclasts is an important role. It is known that Focal adhesion kinase (FAK) is activated by chemokines, cytokines and engagement with β-1 integrin. Fibronectin is decreased in chronically inflamed connective tissue, such as periodontitis. Focal adhesion kinase (FAK) is a 125-kDa non-receptor type tyrosine kinase that localizes to focal adhesions. FAK is involved in osteoclast bone resorption. Fibronectin is bound to &alpha4 β1-integrin and alpha;5 β1-integrin.
In our present study we focused on fibronectin / integrin-mediated the differentiation into osteoclasts and found that this type of the differentiation was medi-ated through FAK. RANKL stimulation did not enhance the expression of α4, α5 and β1-integrin. Fibronectin inhibited RANKL-induced osteoclasts differentiation in RAW264.7 cells. Fibronectin induced the phosphorylation of FAK. These findings establish fibronectin regulate the differentiation into osteoclasts in bone.
Key words: osteoclast, FAK, Fibronectin, RANKL