Abstract
ObjectiveBone resorption mediated by osteoclast differentiation induces the occurrence of bone-related diseases. Macrophages, an origin of osteoclasts, whose M2 type can reduce inflammation-induced bone damage. We aimed to investigate the effect of M2 macrophage-derived exosomes on osteoclast formation and elucidate its underlying mechanism. Materials and MethodsExosomes were isolated from M2 macrophages (M2-exo) and were used to treat osteoclast-like cells. Osteoclast formation was evaluated using tartrate-resistant acid phosphatase, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blotting. The molecular mechanism of M2-exo function was analyzed by qRT-PCR, phosphor-kinase array analysis, and Western blotting. ResultsM2-exo was internalized by osteoclasts and inhibited osteoclast differentiation in vitro. Moreover, CYLD was highly expressed in M2 macrophages and M2-exo-treated osteoclasts, and knockdown of it abrogated the inhibition of osteoclast differentiation caused by M2-exo. Additionally, CYLD suppressed the phosphorylation of STAT3, and STAT3 activator colivelin reversed the inhibition of osteoclast differentiation induced by CYLD overexpression. ConclusionM2-exo inhibits osteoclast differentiation via delivering CYLD, which inactivates STAT3 signaling. These findings may provide a novel therapeutic option for bone diseases including periodontitis.
Published Version
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