Research Paper Volume 14, Issue 1 pp 253—271
Increased expression of osteopontin in subchondral bone promotes bone turnover and remodeling, and accelerates the progression of OA in a mouse model
Figure 4. OPN regulates OA subchondral bone metabolism and accelerates subchondral bone remodeling. (A) Immunostaining of OCN+ cells in the tibial subchondral bone of an OA mouse model treated with vehicle, rmOPN or neutralizing antibody, and sham group. Positive cells were indicated with arrows, scale bars = 100 μm, n=6. (B) ALP staining and western blot analysis of collagen 1α (COL1α), RUNX2, and OCN expression of MC3T3-E1 cells treated with Dex (10−7 M), β-glycerophosphate (10 mM) and VC (50 μg/ml) followed by the stimulation with rmOPN and OPN antibody for 3 or 5 days. (C) ALP activity of MC3T3-E1 cells treated with Dex (10−7 M), β-glycerophosphate (10 mM) and VC (50 μg/ml) followed by the stimulation with rmOPN and antibody for 3 or 5 days, n=6. (D) Representative 3D reconstruction of micro-CT images of the tibial subchondral bone of an OA mouse model treated with vehicle, rmOPN or antibody, and sham group. Osteophyte were indicated with arrows, scale bar = 1 mm. Quantitative analysis of bone volume/total volume (BV/TV) and trabecular thickness (Tb. Th.), n=6. Data are shown as mean ± s. d. and were analyzed by one-way ANOVA, *P < 0.05, **P < 0.01.