Adiponectin inhibits osteoclastogenesis by suppressing NF-κB and p38 signaling pathways

Adiponectin (APN) has been shown to play a key role in regulating bone mineral density (BMD). Nevertheless, the effects of APN on receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation and mechanism of regulation are not entirely clear. The study, therefore, aimed to evaluate the ef...

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Veröffentlicht in:Biochemical and biophysical research communications 2018-09, Vol.503 (3), p.2075-2082
Hauptverfasser: Chen, Guiping, Huang, Leitao, Wu, Xia, Liu, Xuqiang, Xu, Qiang, Li, Fan, Dai, Min, Zhang, Bin
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Sprache:eng
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Zusammenfassung:Adiponectin (APN) has been shown to play a key role in regulating bone mineral density (BMD). Nevertheless, the effects of APN on receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation and mechanism of regulation are not entirely clear. The study, therefore, aimed to evaluate the effect of APN on osteoclastogenesis. Our results showed that APN inhibits osteoclastogenesis and resorption function in vitro by suppressing nuclear factor-κB (NF-κB) and p38 signaling pathways, which is essential for osteoclast formation. Moreover, APN blocked the formation of F-actin rings and attenuated osteoclast-mediated bone resorptive function. Therefore, we concluded that APN may provide a potential treatment for osteoclast-related diseases, such as osteoporosis. •Adiponectin inhibits osteoclastogenesis and resorption function in vitro.•Adiponectin suppresses osteoclastogenesis mainly by inhibition of the NF-κB and p38 signaling pathways.•Adiponectin may provide a potential treatment for osteoclast-related diseases,such as osteoporosis.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2018.07.162