Figure 4: The effects of genetic overexpression of Smad1 within osteoblast on bone formation and Smad-dependent BMP signaling in glucocorticoid-treated mice. | Scientific Reports

Figure 4: The effects of genetic overexpression of Smad1 within osteoblast on bone formation and Smad-dependent BMP signaling in glucocorticoid-treated mice.

From: Targeting osteoblastic casein kinase-2 interacting protein-1 to enhance Smad-dependent BMP signaling and reverse bone formation reduction in glucocorticoid-induced osteoporosis

Figure 4

(a) Schematic diagram of the experimental design. (b) Representative in vivo micro-CT images of the time-course changes in three-dimensional trabecular architecture of the left proximal tibiae from each group. Scale bar: 100 um. (c) The time-course changes in micro-CT parameter (BMD) of the left proximal tibia from each group. (d) Representative micrographs of newly mineralized bone assessed by xylenol (red) and calcein (green) labeling at the left proximal tibiae from each group after 4 weeks. Scale bar: 50 μm. (e) The changes in the bone histomorphometric parameter (MAR and Ob.S/BS) of the left proximal tibiae from each group after 4 weeks. (f) The representative immunofluorescence images for the time-course changes in the co-expression of p-Smad1/5 (green) and OCN + (red) cells of the right proximal tibiae from each group. Merged images with DAPI staining showed cells co-staining of p-Smad1/5 with Osteocalcin (arrow indicated). Scale bar: 25 μm. Note: The data were mean ± s.d. *P < 0.05 for Control-PNL group vs Osx/Smad1-PNL group. Control: Osx-Cre mice; Osx/Smad1: osteoblast-specific Smad1 knock-in mice. Base: Baseline of before glucocorticoid treatment. PNL: prednisolone treatment; VH: Vehicle treatment.

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