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FGFR3 deficient mice have accelerated fracture repair

Bone fracture healing is processed through multiple biological stages that partly recapitulates the skeletal development process. FGFR3 is a negative regulator of chondrogenesis during embryonic stage and plays an important role in both chondrogenesis and osteogenesis. We have investigated the role...

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Autores principales: Xie, Yangli, Luo, Fengtao, Xu, Wei, Wang, Zuqiang, Sun, Xianding, Xu, Meng, Huang, Junlan, Zhang, Dali, Tan, Qiaoyan, Chen, Bo, Jiang, Wanling, Du, Xiaolan, Chen, Lin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599908/
https://www.ncbi.nlm.nih.gov/pubmed/28924384
http://dx.doi.org/10.7150/ijbs.19309
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author Xie, Yangli
Luo, Fengtao
Xu, Wei
Wang, Zuqiang
Sun, Xianding
Xu, Meng
Huang, Junlan
Zhang, Dali
Tan, Qiaoyan
Chen, Bo
Jiang, Wanling
Du, Xiaolan
Chen, Lin
author_facet Xie, Yangli
Luo, Fengtao
Xu, Wei
Wang, Zuqiang
Sun, Xianding
Xu, Meng
Huang, Junlan
Zhang, Dali
Tan, Qiaoyan
Chen, Bo
Jiang, Wanling
Du, Xiaolan
Chen, Lin
author_sort Xie, Yangli
collection PubMed
description Bone fracture healing is processed through multiple biological stages that partly recapitulates the skeletal development process. FGFR3 is a negative regulator of chondrogenesis during embryonic stage and plays an important role in both chondrogenesis and osteogenesis. We have investigated the role of FGFR3 in fracture healing using unstabilized fracture model and found that gain-of-function mutation of FGFR3 inhibits the initiation of chondrogenesis during cartilage callus formation. Here, we created closed, stabilized proximal tibia fractures with an intramedullary pin in Fgfr3(-/-)mice and their littermate wild-type mice. Fracture healing was evaluated by radiography, micro-CT, histology, and real-time polymerase chain reaction (RT-PCR) analysis. The fractured Fgfr3(-/-) mice had increased formation of cartilaginous callus, more fracture callus, and more rapid endochondral ossification in fracture sites with up-regulated expressions of chondrogenesis related gene. The fractures of Fgfr3(-/-) mice healed faster with accelerated fracture callus mineralization and up-regulated expression of osteoblastogenic genes. The healing of fractures in Fgfr3(-/-) mice was accelerated in the stage of formation of cartilage and endochondral ossification. Downregulation of FGFR3 activity can be considered as a potential bio-therapeutic strategy for fracture treatment.
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spelling pubmed-55999082017-09-18 FGFR3 deficient mice have accelerated fracture repair Xie, Yangli Luo, Fengtao Xu, Wei Wang, Zuqiang Sun, Xianding Xu, Meng Huang, Junlan Zhang, Dali Tan, Qiaoyan Chen, Bo Jiang, Wanling Du, Xiaolan Chen, Lin Int J Biol Sci Research Paper Bone fracture healing is processed through multiple biological stages that partly recapitulates the skeletal development process. FGFR3 is a negative regulator of chondrogenesis during embryonic stage and plays an important role in both chondrogenesis and osteogenesis. We have investigated the role of FGFR3 in fracture healing using unstabilized fracture model and found that gain-of-function mutation of FGFR3 inhibits the initiation of chondrogenesis during cartilage callus formation. Here, we created closed, stabilized proximal tibia fractures with an intramedullary pin in Fgfr3(-/-)mice and their littermate wild-type mice. Fracture healing was evaluated by radiography, micro-CT, histology, and real-time polymerase chain reaction (RT-PCR) analysis. The fractured Fgfr3(-/-) mice had increased formation of cartilaginous callus, more fracture callus, and more rapid endochondral ossification in fracture sites with up-regulated expressions of chondrogenesis related gene. The fractures of Fgfr3(-/-) mice healed faster with accelerated fracture callus mineralization and up-regulated expression of osteoblastogenic genes. The healing of fractures in Fgfr3(-/-) mice was accelerated in the stage of formation of cartilage and endochondral ossification. Downregulation of FGFR3 activity can be considered as a potential bio-therapeutic strategy for fracture treatment. Ivyspring International Publisher 2017-07-18 /pmc/articles/PMC5599908/ /pubmed/28924384 http://dx.doi.org/10.7150/ijbs.19309 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Xie, Yangli
Luo, Fengtao
Xu, Wei
Wang, Zuqiang
Sun, Xianding
Xu, Meng
Huang, Junlan
Zhang, Dali
Tan, Qiaoyan
Chen, Bo
Jiang, Wanling
Du, Xiaolan
Chen, Lin
FGFR3 deficient mice have accelerated fracture repair
title FGFR3 deficient mice have accelerated fracture repair
title_full FGFR3 deficient mice have accelerated fracture repair
title_fullStr FGFR3 deficient mice have accelerated fracture repair
title_full_unstemmed FGFR3 deficient mice have accelerated fracture repair
title_short FGFR3 deficient mice have accelerated fracture repair
title_sort fgfr3 deficient mice have accelerated fracture repair
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599908/
https://www.ncbi.nlm.nih.gov/pubmed/28924384
http://dx.doi.org/10.7150/ijbs.19309
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