CKIP-1 silencing promotes new bone formation in rat mandibular distraction osteogenesis

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• 作者：Zi-chao Zhou ; BS^a ; Lei Che ; MPH^b ; ^c ; Liang Kong ; DDS ; PhD^d ; De-lin Lei ; DDS^d ; Rui Liu ; MS^e ; Xin-jie Yang ; DDS ; PhD^d ; ^{Yangxinjie@fmmu.edu.cn}
• 刊名：Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：123
• 期：1
• 页码：e1-e9
• 全文大小：2907 K
• 卷排序：123

文摘

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 DesignCKIP-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.ResultsGross 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.ConclusionsPromotion of bone formation after CKIP-1 silencing in rat mandibular distraction osteogenesis appears to be mediated through the Wnt3 a/β-catenin signaling pathway.