Zi-Chao Zhou1, Lei Che2, Liang Kong3, De-Lin Lei3, Rui Liu4, Xin-Jie Yang5. 1. First Cadet Brigade, Fourth Military Medical University, Xi'an, China. 2. State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, and Shaanxi Key Laboratory of Oral Diseases, Department of Prosthodontics, School of Stomatology, Fourth Military Medical University, Xi'an, China; Department of Military Preventive Medicine, Fourth Military Medical University, Xi'an, China. 3. State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, and Shaanxi Clinical Research Center for Oral Diseases, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, China. 4. State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Nursing Department, School of Stomatology, Fourth Military Medical University, Xi'an, China. 5. State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, and Shaanxi Clinical Research Center for Oral Diseases, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi'an, China. Electronic address: Yangxinjie@fmmu.edu.cn.
Abstract
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.
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.