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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: J Cell Physiol. 2016 Feb;231(2):449–458. doi: 10.1002/jcp.25091

Fig.2. The role of FcγRIIa in IVIG-induced suppression of osteoclastogenesis.

Fig.2

(a and b) Human monocytes were nucleofected with control or FcγRIIa-specific small interfering RNAs (siRNAs). (a) FcγRIIa knock-down efficiency was measured by RT-qPCR and normalized relative to the expression of GAPDH. ***p < 0.001 by paired t-test. (b) TRAP-positive, multinucleated osteoclast formation was visualized by TRAP staining. Left panel, Representative results. Right panel, Values are the mean ± SEM from three experiments. The number of osteoclasts obtained from control siRNA is set as 100%. *p < 0.05, **p < 0.01, ***p < 0.001 by one-way ANOVA. (c-d) Down-regulation of mRNA and cell surface expression of Fcγ receptors by IVIG. (c and d) Human monocytes were cultured for one day with human M-CSF (20 ng/ml). (c) Cells were cultured with human RANKL (40ng/ml) for the indicated times and mRNA was measured by RT-qPCR. mRNA of Fcγ receptors was normalized relative to the expression of GAPDH. Values are the mean ± SEM. *;P=0.05, **: P < 0.01, *** ;P < 0.001. (d) RANKL (40ng/ml) was added to the culture for 36 hrs. Surface expression of Fcγ receptors was measured by flow cytometry. Dotted line represents an isotype control. Gray shaded are corresponds to control cells and the thick line represents IVIG treated cells. Left panel: Representative histograms from five experiments are shown. Right panel: MFI of control cells was set as 100% and mean % of inhibition of surface expression of proteins was shown.