Tissue & cell · 2024
Exosomes secreted from M2-polarized macrophages inhibit osteoclast differentiation via CYLD.
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Guo Zi-Yan, Yin Nan-Nan, Li Xiao-Fei, Wang Meng-Meng, Sui Xiao-Na, Jiang Cai-di, Xu Ming-Hua, Jia Xiao-E, Fu Chong-Jian, Chen Tie-Lou, Liu Xin
Аннотация
OBJECTIVE: Bone 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 METHODS: Exosomes 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.
RESULTS: M2-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.
CONCLUSION: M2-exo inhibits osteoclast differentiation via delivering CYLD, which inactivates STAT3 signaling. These findings may provide a novel therapeutic option for bone diseases including periodontitis.
MATERIALS AND METHODS: Exosomes 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.
RESULTS: M2-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.
CONCLUSION: M2-exo inhibits osteoclast differentiation via delivering CYLD, which inactivates STAT3 signaling. These findings may provide a novel therapeutic option for bone diseases including periodontitis.