PDLIM3 Antibody - #DF12525

Fig. 9 (A) Masson staining: the region between surrounding bone and scaffold (40x & 100x); (B) TRAP staining: TRAP positive cells (black arrows); (C) IHC staining of RUNX-2; (D) IHC staining of ALP; (E) Quantitative analysis for TRAP staining and IHC staining. * Compared with CPS group; # compared with Sr-5 group.

Figure 5. In vitro biocompatibilities and osteogenic activities of the substrates. (A) CCK-8 assay of hBMSCs on the indicated surfaces after 1, 3 and 7 days of culture. * denotes p < 0.05 and ** denotes p < 0.01 compared to Ti-NTs, # denotes p < 0.05 compared to the corresponding control group without peptides. Error bars denote the standard deviations over quadruplicate measurements with separately implants. (B) Confocal fluorescence microscopy images of hBMSCs stained with vinculin, F-actin and DAPI after being cultured for 24 h. Scale bar, 50 μm. (C-F) qRT-PCR assay of osteogenic gene expression of (C) ALP, (D) RUNX-2, (E) COL1 and (F) OPN of hBMSCs after 7 and 14 days of culture. * denotes p < 0.05, ** denotes p < 0.01 and *** denotes p < 0.001 compared to Ti-NTs-P-A; # denotes p < 0.05, & denotes p < 0.01 and $ denotes p < 0.001 compared to the corresponding control group without peptides. All error bars denote the standard deviations over quadruplicate measurements with separately implants. (G) Immunofluorescence staining of hBMSCs cultured on Ti-NTs-P-A for 7 days (ALP and RUNX-2) and 14 days (OPN). The images were obtained by confocal fluorescence microscopy. Scale bar, 50 μm. (H) Western blotting of hBMSCs cultured on the substrates for 7 and 14 days. At each time point, left lane was Ti-NTs, middle lane was Ti-NTs-A and right lane was Ti-NTs-P-A. * denotes p < 0.05, ** denotes p < 0.01 and *** denotes p < 0.001 compared to Ti-NTs-P-A. Error bars denote the standard deviations over triplicate measurements with separately Western blotting results.

Fig. 3 10− 6 M insulin promotes the osteogenic differentiation of human DPSCs. A 10− 6 M insulin up-regulated the mRNA levels of COL-1, ALP, OCN, and RUNX2 in DPSCs at day 3 and day 7 (n = 3). B 10− 6 M insulin promoted the protein expressions of COL-1, ALP, OCN, and RUNX2 in DPSCs at day 7 (n = 3). Representative western blotting (left) and quantification analysis (right). Full-length blots/gels are presented in Supplementary Fig. 1. C 10− 6 M insulin increased the secretion of extracellular bone metabolism and biochemical markers in DPSCs at day 1–7 and day 7–14 (n = 6). D 10− 6 M insulin enhanced alkaline phosphatase staining of DPSCs at day 21 (scale bars: 100 μm). E 10− 6 M insulin enhanced Alizarin red staining of DPSCs at day 21 (scale bars: 100 μm). F 10− 6 M insulin promoted the mineralized matrix formation of DPSCs at day 21 (n = 6). Data are expressed as the mean ± SD. *P 

Fig. 4 |Inactivation of ERK/MAPK signaling pathway inhibited the odontogenic differentiation of BMMSCs induced by TGC-CM. a ERK inhibitor U0126 significantly inhibited the mineralization and b reduced ALP, DSP, and DMP-1 protein levels of BMMSCs during odontogenic differentiation induced by TGC-CM for 7 days. Scale bar = 100 μm

FIGURE 6. Immunohistochemical staining of ALP, COL1, OCN, and RUNX2 after implantation for 4 and 8 weeks.