Fig. 7

Knockdown of CDR1as inhibited bone formation in vivo. a Reconstructed three-dimensional micro-CT images of the calvarial defect area of nude mice contained normal control (NC) and small interfering RNA (si)-CDR1as treated PDLSCs. The histograms show the bone mineral density (BMD; left panel) and the ratio of new bone volume to existing tissue volume (BV/TV; right panel) of the two groups. b Hematoxylin and eosin (H&E) staining in NC and si-CDR1as groups. Bone formation (B) around the scaffold (S) and the original cranial bones (C) were identified. Scale bar = 100 μm. c Confocal microscopy of osteocalcin (OCN) with DAPI counterstaining in NC and si-CDR1as groups in the calvarial defect area. Scale bars = 50 μm. d Schematic illustration showed the signaling of CDR1as/miR-7/GDF5/Smad and p38 MAPK in PDLSCs. CDR1as relieved the negative regulation of miR-7 on growth differentiation factor 5 (GDF5) by acting as an miR-7 sponge and subsequently activated the pSmad1/5/8 and p38 MAPK (p38) pathway