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. 2019 Oct 17;20(20):5141. doi: 10.3390/ijms20205141

Figure 5.

Figure 5

Analysis of TNFSF13b immunohistochemistry and action in osteoclast formation. Bone cells in glucocorticoid-treated WT mice showed strong TNFSF13b immunostaining, but expressed weak immunoreaction in glucocorticoid-treated miR-29aTg mice (A); scale bar, 10 μm. miR-29a overexpression attenuated the glucocorticoid-induced increases in TNFSF13b immunostaining (B) and serum TNFSF13b levels (C). TNFSF13b antibody blockade attenuated the glucocorticoid-induced osteoclast formation of bone-marrow macrophages from WT mice, whereas TNFSF13b protein increased osteoclast formation of bone-marrow macrophages from glucocorticoid-treated miR-29aTg mice (D); scale bar, 8 μm. Data are expressed as the mean ± standard errors calculated from 6 mice. Asterisks * indicate significant differences from the WT + Veh group, hashtags # indicate significant differences from the WT + GC group and plus + indicate significant difference the Tg + GC group (p < 0.05). WT, wild-type mice; Tg, miR-29aTg mice; Veh, vehicle; GC, glucocorticoid; TNFSF13b, tumor necrosis factor superfamily 13b; Ab, antibody.