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CKIP-1 silencing promotes new bone formation in rat mandibular distraction osteogenesis.
OBJECTIVE: This study investigated the effects and possible molecular mechanism of casein kinase-2 interacting protein-1 (CKIP-1) silencing on bone regeneration during rat mandibular distraction osteogenesis (DO).
STUDY DESIGN: CKIP-1 silencing by chitosan/si-CKIP-1 was employed and analyzed both in rat mandibular DO models in vivo and in cultured rat mandible bone marrow stromal cells (BMSCs) in vitro.
RESULTS: Gross observation, micro-computed tomography analysis, and hematoxylin and eosin (H&E) staining revealed that new bone formation in the distraction gap of the chitosan/si-CKIP-treated group was better compared with the chitosan/si-NC and phosphate buffered saline-treated groups in both quantity and quality. Proliferation assay, flow cytometry, and alizarin red staining indicated that CKIP-1 silencing significantly inhibited apoptosis, but promoted osteogenic differentiation of cultured BMSCs. Additionally, CKIP-1 silencing significantly promoted the expression of Wnt3 a, β-catenin, and osteocalcin both in new bone formation of DO models in vivo and in the osteogenic differentiation process of BMSCs in vitro.
CONCLUSIONS: Promotion of bone formation after CKIP-1 silencing in rat mandibular distraction osteogenesis appears to be mediated through the Wnt3 a/β-catenin signaling pathway.
STUDY DESIGN: CKIP-1 silencing by chitosan/si-CKIP-1 was employed and analyzed both in rat mandibular DO models in vivo and in cultured rat mandible bone marrow stromal cells (BMSCs) in vitro.
RESULTS: Gross observation, micro-computed tomography analysis, and hematoxylin and eosin (H&E) staining revealed that new bone formation in the distraction gap of the chitosan/si-CKIP-treated group was better compared with the chitosan/si-NC and phosphate buffered saline-treated groups in both quantity and quality. Proliferation assay, flow cytometry, and alizarin red staining indicated that CKIP-1 silencing significantly inhibited apoptosis, but promoted osteogenic differentiation of cultured BMSCs. Additionally, CKIP-1 silencing significantly promoted the expression of Wnt3 a, β-catenin, and osteocalcin both in new bone formation of DO models in vivo and in the osteogenic differentiation process of BMSCs in vitro.
CONCLUSIONS: Promotion of bone formation after CKIP-1 silencing in rat mandibular distraction osteogenesis appears to be mediated through the Wnt3 a/β-catenin signaling pathway.
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