Abstract: Objective To investigate the molecular mechanisms of hydatid antigen-B (Hyd-B) in osteoclastogenesis. Methods Cell experiment group-1: Bone marrow mesenchymal stem cells(BMSCs) were divided into 3 groups (Control group, MCSF + RANKL group, MCSF + RANKL + Hyd-B group), cells in the MCSF + RANKL group and MCSF + RANKL + Hyd-B group were induced to differentiate into osteoclasts by using macrophage colony-stimulating factor (MCSF) combined with soluble receptor activator of nuclear factor-κb ligand (RANKL), and then treated with or without Hyd-B respectively. Cell experiment group-2: BMSCs were divided into Ctrl group and Hyd-B treatment group (Treat group), the effect of Hyd-B on the direct interaction between TAZ and TAK1 was determined by co-immunoprecipitation ( co-IP). IP was performed by using antiTAK1 antibody, and TAZ expression level was detected by IB. Cell experiment group-3: BMSCs were divided into 5 groups: Control group, MCSF + RANKL group, MCSF + RANKL + Hyd-B group, MCSF + RANKL + Hyd-B + TAZ-OE group and MCSF + RANKL + Hyd-B + OE-vector group. TAZ overexpression plasmid or vector plasmid was transfected to the BMSCs in the MCSF + RANKL + Hyd-B + TAZ-OE group and MCSF + RANKL + Hyd-B + OE-vector group respectively. qPCR was used to detect the mRNA expression levels of osteoclast differentiation markers of TRAP and Cathepsin K. Western blotting was used to detect the expression levels of nuclear p-P65, cytoplasmic P65, nuclear NFATc1, p-AKT, AKT, p-ERK 1 / 2, ERK 1 / 2, p-TAZ, TAZ and TAK1. Results Compared with those in the Control group, the TRAP and Cathepsin K mRNA expression levels in the MCSF + RANKL and MCSF + RANKL + Hyd-B groups were increased (P <0. 05); the expression levels of p-P65, p-AKT and p-ERK 1 / 2 were increased (P < 0. 05); theexpression levels of p-P65 and NFATc1 in nucleus were increased (P < 0. 05). The expression levels of the above indicators were further increased in the MCSF + RANKL + Hyd-B group when compared with those in the MCSF + RANKL group ( P < 0. 05). Compared with those in the MCSF +RANKL + Hyd-B group, the expression levels of the above indicators in MCSF + RANKL + Hyd-B +TAZ-OE group were all reduced (P < 0. 05). Co-IP results showed that Hyd-B treatment enhancedthe interaction between TAZ and TAK1 ( P < 0. 05). Compared with those in the Ctrl group, thephosphorylated level of cytoplasmic TAZ in Treat group was increased, the expression level of TAZwas reduced (P< 0. 05). Conclusion Hyd-B can promot the RANKL / NF-κB / TAK1-mediated osteoclastogenesis through inhibition of TAZ.

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