Fig. 1: Irgm1 is correlated with osteoporosis and osteoclast differentiation.

A WB showed the expression of Irgm1 in BMDMs. Quantitative data were normalized to GAPDH and presented as means ± SD. ^∗∗∗p < 0.001 vs the indicated groups. B Volcano diagram displayed that Irgm1 was continuously upregulated during osteoclast differentiation mediated by RANKL at days 1, 2, and 3. C Venn diagram summarizes 82 candidate targets of RANKL-induced osteoclast differentiation at days 1, 2, and 3. D–F GO enrichment analysis to identify the top 10 significant terms of cell component (D), biological process (E), and molecular function (F), corresponding to the candidate targets. G KEGG pathway analysis suggested potential signaling pathways by which Irgm1 regulated osteoclast differentiation. H WB analysis of Irgm1 expression in RANKL-induced BMDMs. Cells were treated with RANKL (40 ng/ml) and M-CSF (10 ng/ml) for 0, 1, 3, and 5 days. Quantitative data were normalized to GAPDH and presented as means ± SD (n = 3). ^∗∗∗p < 0.001, ^##p < 0.01, and ^†††p < 0.001 vs 0 group. I WB analysis of Irgm1 expression after treatment with different concentrations of RANKL (0, 40, 80 ng/ml) for 3 days. Quantitative data were normalized to GAPDH and presented as means ± SD (n = 3). ^∗∗p < 0.01 and ^##p < 0.01 vs 0 group. J Immunohistochemical staining images of bone tissues from the osteoporosis and healthy (Control) group. Scale bar = 100 μm. Quantitative analysis of the immunohistochemical staining and presented as means ± SD. ^∗∗∗p < 0.001 vs the control group.