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Achondroplasia(ACH) is the most common form of dwarfism caused by activated mutations of FGFR3 gene.Gain-of-function mutation of FGFR3 in mice (FGFR3G369C/+ mice, ACH mice) resulted in delayed fracture healing by inhibiting chondrocyte differentiation and bone resorption.The expression of PTHrP in callus is lower in ACH.Researches have demonstrated that PTH1-34 preferentially enhanced chondrocyte recruitment the rate of chondrocyte maturation to stimulate endochondral ossification.In this study, we explored the effect of PTH1-34 on the delayed fracture healing resulting from ACH.Closed fracture of proximal tibia was created and stabilized with an intramedullary pin in 7-8-week-old mice.The mice were randomly divided into treatment and control group.The mice in treatment group were given PTH1-34 80μg/(kg·d) subcutaneously until the end of observation period while the controls were given sterile water.Callus tissues were analyzed by radiography and histology.RNA was isolated from callus tissues, and the expression levels of bone formation-related genes were evaluated by real-time PCR.At 7 days post-fracture(PF), cartilaginous callus areas were increased in PTH1-34-treated ACH mice compared with those of control mice.In contrast, at PF14, the remnant cartilaginous callus areas were smaller in PTH-treated mice than those in control mice.Remnant cartilaginous callus in ACH control mice were obverse,while little remnant cartilaginous callus was observed at PF21.The remnant fibrous bone areas in marrow cavity were also reduced in PTH-treated mice compared to control mice at PF28.In the early stages of fracture, compared with the control group, the PCNA and COL10A1 mRNAs expression were obviously increased in PTH1-34 treatment group.In the middle stages of fracture, compared with the control group, the OC mRNA expression level were significantly increased in PTH1-34 treatment group.These results suggested that PTH1-34 promoted bone fracture healing in terms of increasing callus areas, endochondral ossification.