The ameloblastin extracellular matrix molecule enhances bone fracture resistance and promotes rapid bone fracture healing
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- 作者：Xuanyu Lua ; b ; Wenjin Lic ; Satoshi Fukumotod ; Yoshihiko Yamadad ; Carla A. Evansb ; Tom Diekwischa ; e ; diekwisch@bcd.tamhsc.edu" class="auth_mail" title="E-mail the corresponding author ; Xianghong Luana ; b ; luan@uic.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：Ameloblastin ; Bone fracture ; Fracture healing ; Mesenchymal stem cells ; Proliferation
- 刊名：Matrix Biology
- 出版年：2016
- 出版时间：May-July 2016
- 年：2016
- 卷：52-54
- 期：Complete
- 页码：113-126
- 全文大小：2625 K
文摘
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Lack of a functional AMBN in the bone matrix resulted in 31% decreased femur bone mass and 40% reduced energy to failure.
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AMBN function inhibition diminished the proliferative capacity of fracture repair callus cells.
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AMBN truncation was associated with an enhanced and prolonged chondrogenic phase.
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There was a 6.9-fold increase in AMBN expression at the fracture site one week after fracture.
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Application of exogenous AMBN protein to bone fracture sites accelerated callus formation and bone fracture healing.