Identification and characterization of osteoclast-derived coupling factor

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Bone remodeling is regulated by a coupling of resorption to subsequent formation, however, the "coupling factor" and underlying mechanism are not fully understood. I purified osteoblast-stimulating activity, as determined by ALP activity, from osteoclast CM through successive chromatography by monitoring the ALP activity, and identified complement component 3 (C3). The activity present in osteoclast CM was inhibited by a specific C3a receptor antagonist, SB290157. C3 gene expression in bone was increased in the high bone turnover states of ovariectomy (OVX) or a RANKL injection, and blocking the action of C3a with the daily administration of SB290157 resulted in the attenuation of bone formation elevated by OVX, and the exacerbation of bone loss. These results suggest that osteoclast-derived C3a functions in the relay from bone resorption to formation and may be a candidate for a coupling factor.