The effect of FcγRs on the CRP-induced osteoclastogenesis from monocytes. (A) CD14+ monocytes, which were isolated from peripheral blood, were cultured with 25 ng/mL of M-CSF and 1.0 μg/mL of CRP in the presence of anti-CD64 (FcγRI inhibitor), anti-CD32 (FcγRIIa inhibitor), or anti-CD16 (FcγRIIb inhibitor). After 21 days of culture, TRAP+ multinucleated cells were counted. The inhibition of FcγRI, FcγRIIa, and FcγRIIb decreased CRP-induced osteoclastogenesis. The figure represents one of three independent experiments (original magnification: 200×). (B) The gene expression of osteoclast fusion proteins such as DC-STAMP and MFR were measured from differentiated osteoclasts using real-time PCR. The expression of DC-STAMP decreased significantly with the inhibition of FcγRI, FcγRIIa, and FcγRIIb, and the expression of MFR decreased significantly with the inhibition of FcγRI and FcγRIIa. (C) The gene expressions of osteoclast markers such as cathepsin K, RANK, MMP-9, and CTR were measured from differentiated osteoclasts using real-time PCR. The gene expressions of cathepsin K, RANKL, and MMP-9 decreased significantly with the inhibition of FcγRI, FcγRIIa, and FcγRIIb. The expression of CTR mRNA decreased with the inhibition of FcγRI. The data represents the mean ± SEM for three independent experiments; *
P <0.05 and **
P <0.01. CRP, C-reactive protein; CTR, calcitonin receptor; DC-STAMP, dendritic cell-specific transmembrane protein; FcγR, Fcgamma receptors; M-CSF, macrophage colony-stimulating factor; MFR, macrophage fusion receptor; MMP, matrix metalloproteinases; RANKL, receptor activator of nuclear factor kappa-B ligand; SEM, standard error of the mean.