(A–D) Immunoblot analysis of type-I IFN receptor expression during osteoblast differentiation (A), the induction of p-STAT1 and 3 (B, C) and expression of STAT1 (D) in WT and Def6-/- osteoblast cells stimulated with mouse recombinant IFN-β (10 U/ml) at the indicated time points. p38 was used as a loading control. The relative density of each band to its corresponding loading control p38 band was calculated by Image J software, and then was normalized to the WT controls at time 0 (the 1st lanes). The relative density for p-STAT3 to total STAT3 was also calculated. (E) qPCR analysis of type-I IFN response gene expression after indicated time points of treatment with IFN-β (10 U/ml) in WT and Def6-/- osteoblast cells. (F) Osteoblast differentiation is induced by the osteogenic medium in the absence or presence of mouse recombinant IFN-β in the WT and Def6-/- osteoblast cells. Alizarin red staining at day 16 (left panel) and its quantification (right panel) were performed. Data are mean ± SEM. *p<0.05, **p<0.01. n.s., not statistically significant. (G) A model showing that the Def6-IFN axis regulates both osteoclast-mediated bone resorption (Binder et al., 2017) and osteoblast-mediated bone formation (current study) in bone homeostasis. Def6 deletion enhances both bone resorption (Binder et al., 2017) and formation (current study) via attenuated type-I IFN-mediated feedback inhibition of the differentiation of both cell types, leading to a high turn-over osteoporotic phenotype in Def6-/- mice.
Figure 5—source data 1. Source data for Figure 5.