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- Title
Jmjd3和Ezh2拮抗调节小鼠骨折愈合.
- Authors
王新力; 王钰莹; 赵雄; 王冠杰; 汪钰; 张鑫; 张冉; 张之岩; 杨博; 马福浩; 许宏业; 武晓慧; 雷伟; 张丰
- Abstract
Objective: To investigate the roles of Jmjd3 and H/h2 in the processes of bone fracture healing in mice. Methods: Mice with gene conditional knockout (cKO)in chondrocytes were used in this study. Male mice at 8-10 weeks old were randomly divided into 6 groups according to their genotypes, with 5 mice in each group. Mice with Jmjd3fl/fl/Col2al-CreERT2, Ezh2fl/fl/Col2al-CreERT2Jmjd3fl/fl/Ezh2fl/fl/Col2al-CreERT2 genotypes were experimental groups. Mice with Jmjd3fl/fl, Ezh2fl/fl or Jmjdfl/fl/Ezh2fl/fl genotypes were control groups. The mice were given a unilateral open tibiae transverse fracture operation with intramedullary' needle fixation under aseptic condition. At 3. 5 and 7 days after the operation, the mice were intraperitoneally injected tamoxifen (3 nig per day for each time) and were sacrificed 3 weeks later for X ray and histology investigations. Results: X ray scanning and histology measurement showed that the most suitable time for observing the results of bone fracture healing in mice was at the third week after operation. At this stage. X ray showed that the fracture line in Jmjd3 cKO mice is clearer than the controlled group. Meanwhile, the ossified callus of Jmjd3 cKO group is much smaller and has lower density compared with the controlled group. HE tissue slices showed that the cKO group had significantly less ossified callus and more cartilage callus than the controlled group. In contrast, the X ray showed that the callus of Lzli2 cKO group was larger and had higher density than the controlled group. HE tissue slices showed that the calcification of ossified callus was higher in the cKO group. Besides, the trabecular bone of the cKO group was thicker and more dense. Lastly, the X ray and HE tissue slices showed that no significant difference were observed between Jmjd3Hzh2 double cKO and controlled group. Conclusion: Based on gene cKO mice, we firstly detected that Jmjd3 can facilitate but ii/iil suppress bone fracture healing in mice. We also find (hat Jsnjd3 and Bzh2 counteractally regulate the process of bone fracture healing in vivo. These findings provide a new molecular experimental basis and implications for fracture healing treatment.
- Publication
Progress in Modern Biomedicine, 2018, Vol 18, Issue 10, p1875
- ISSN
1673-6273
- Publication type
Article
- DOI
10.13241/j.cnki.pmb.2018.10.014