丹麦克朗
软骨内骨化
骨愈合
Wnt信号通路
间充质干细胞
细胞生物学
祖细胞
成骨细胞
信号转导
化学
医学
癌症研究
软骨
干细胞
解剖
生物
生物化学
体外
作者
Hongting Jin,Baoli Wang,Jia Li,Wei‐Fen Xie,Qiang Mao,Shan Li,Feifei Dong,Yan Sun,H.Z. Ke,Philip Babij,Peijian Tong,Di Chen
出处
期刊:Bone
[Elsevier]
日期:2015-02-01
卷期号:71: 63-75
被引量:79
标识
DOI:10.1016/j.bone.2014.07.039
摘要
In this study we investigated if Wnt/β-catenin signaling in mesenchymal progenitor cells plays a role in bone fracture repair and if DKK1-Ab promotes fracture healing through activation of β-catenin signaling. Unilateral open transverse tibial fractures were created in CD1 mice and in β-catenin(Prx1ER) conditional knockout (KO) and Cre-negative control mice (C57BL/6 background). Bone fracture callus tissues were collected and analyzed by radiography, micro-CT (μCT), histology, biomechanical testing and gene expression analysis. The results demonstrated that treatment with DKK1-Ab promoted bone callus formation and increased mechanical strength during the fracture healing process in CD1 mice. DKK1-Ab enhanced fracture repair by activation of endochondral ossification. The normal rate of bone repair was delayed when the β-catenin gene was conditionally deleted in mesenchymal progenitor cells during the early stages of fracture healing. DKK1-Ab appeared to act through β-catenin signaling to enhance bone repair since the beneficial effect of DKK1-Ab was abrogated in β-catenin(Prx1ER) conditional KO mice. Further understanding of the signaling mechanism of DKK1-Ab in bone formation and bone regeneration may facilitate the clinical translation of this anabolic agent into therapeutic intervention.
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