Figure 5: The effect of therapeutic inhibition of CKIP-1 within osteoblast on Smad-dependent BMP signaling and bone formation in glucocorticoid-treated mice. | Scientific Reports

Figure 5: The effect of therapeutic inhibition of CKIP-1 within osteoblast on Smad-dependent BMP signaling and bone formation 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 5

(a) Schematic diagram of the experimental design. (b) The level of CKIP-1 mRNA expression in OCN + cells isolated by LCM from cryosection of proximal tibia in each group. (c) Representative immunofluorescence images for CKIP-1 and pSmad1/5 expression in OCN + cells in cryosection of proximal tibia from each group. Upper panel: CKIP-1, green; OCN, red; Nucleus, blue. Lower panel: pSmad1/5, green; OCN, red; Nucleus, blue. Scale bars: 25 μm. (d) Representative images for three-dimensional trabecular architecture at proximal tibia from each group. Scale bars: 100 μm. (e) Micro-CT parameters for bone mass (BMD, BV/TV) and trabecular architecture (Tb.Th and Tb.N) at proximal tibia from each group. (f) Bone histomorphometric parameters (MAR and Ob.S/BS) at proximal tibia from each group. (g) Representative fluorescence microscopic images of fluorescence-labeling with xylenol orange (red)/calcein green (green) of the left proximal tibiae from each group. Scale bar: 50 um. Note: All data were mean ± s.d. *P < 0.05. n = 8 mice in each group. Baseline: mice sacrificed before glucocorticoid treatment, GIO: mice administrated with phosphate buffer solution (negative control), GIO + Veh: mice administrated with delivery system only, GIO + NC: mice administrated with nonsense RNA negative control with delivery system, GIO + siRNA: mice administrated with CKIP-1 siRNA encapsulated within osteoblast-targeting delivery system, Control: mice that were not treated with glucocorticoid.

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