PTH 1-34 Ameliorates the Osteopenia and Delayed Healing of Stabilized Tibia Fracture in Mice with Achondroplasia Resulting from Gain-Of-Function Mutation of FGFR3

International Journal of Biological Sciences
Hangang ChenZhongliang Deng

Abstract

Bone fracture healing is processed through multiple stages including the cartilaginous callus formation and its transition to bony callus. FGFR3 negatively regulates chondrogenesis and enhances osteogenesis during skeleton development. We previously found in mice carrying gain-of-function mutation of FGFR3 that FGFR3 delays the healing of un-stabilized fracture that heals mainly through endochondral ossification. Since fracture is regularly treated in clinics with rigid fixation, and stabilized fracture is healed largely through intramembranous ossification, we asked whether FGFR3, a key regulator of osteogenesis, also affect the regeneration of stabilized fracture. We found that gain-of-function mutation of FGFR3 inhibits the initiation of chondrogenesis and the subsequent bone formation. We further studied whether PTH1-34 can improve the osteopenia and delayed healing of the stabilized tibia fracture in mice with achondroplasia. Fracture healing was evaluated by radiography, micro-CT, biomechanical tests, histology, and real-time polymerase chain reaction (RT-PCR) analysis. We found that PTH 1-34 can alleviate the decreased bone mass and compromised architecture in ACH mice. Histological analysis revealed that administration ...Continue Reading

Citations

Sep 4, 2020·Signal Transduction and Targeted Therapy·Yangli XieLin Chen
Sep 12, 2020·Stem Cell Reports·Anais JulienCéline Colnot
Jun 9, 2021·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Laura E ZweiflerLaurie K McCauley

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Methods Mentioned

BETA
genotyping
dissection
X-ray
PCR

Software Mentioned

PASW

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