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- W4313349852 abstract "Abstract NF-κB signaling is essential for RANKL-induced osteoclast (OC) formation. IL-4 inhibited RANKL-induced OC differentiation, while at the same time promoted macrophage fusion to form multinucleated giant cells (MNG). Several groups have proposed that IL-4 acted by suppressing the RANKL-induced activation of NF-κB. However, we found that IL-4 did not block canonical NF-κB signaling. Instead, we found that IL-4 inhibited alternative NF-κB signaling and induced p105/50 expression. Interestingly, in p105/50 deficient bone marrow macrophages (BMM), the formation of both multinucleated OC and MNG induced by RANKL or IL-4 respectively was impaired. This suggests that NF-κB signaling also plays an important role during macrophage fusion and MNG formation. To confirm this, the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) was used; PDTC blocked both RANKL-induced OC and IL-4-induced MNG formation. RT-PCR and western blot analyses showed that E-cadherin, and DC-STAMP, proteins important for macrophage fusion, were downregulated by PDTC. Furthermore, overexpression of p52 or RelB in p105/50 deficient BMM significantly enhanced both OC and MNG formation. DC-STAMP was upregulated in p52 and RelB transduced BMMs. These results suggest that the influence of IL-4 on NF-κB activation pathways is complex, and that NF-κB pathways positively regulate the IL-4-induced formation of MNG by MCSF-dependent macrophages." @default.
- W4313349852 created "2023-01-06" @default.
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- W4313349852 date "2010-04-01" @default.
- W4313349852 modified "2023-09-25" @default.
- W4313349852 title "Regulation of the Receptor Activator of NF-κB Ligand (RANKL)-induced activation of the alternative NF-κB pathways by interleukin-4 (IL-4) (142.8)" @default.
- W4313349852 doi "https://doi.org/10.4049/jimmunol.184.supp.142.8" @default.
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