Abstract
Objective To evaluate the effect of Wnt/β-catenin signals on the fracture healing in transgenic mice. Methods Col2al-ICAT transgenic mice were generated by the gene targeting technology with the ICAT transgene specifically expressed in chondrocytes as a competitive inhibitor to block Wnt/ β-catenin signals. The 8-week-old Col2al-ICAT mice were used in the experimental group and the wild type (WT) littermates with the same age served as the control group. A transverse osteotomy was performed at the middle of the tibia and the fracture healing was evaluated on the 7th, 9th, 14th, 21th and 28th days re-spectively after fracture. Roentgenogyaphy and histology observations were performed to evaluate the fracture healing pattern and the histomorphometric analysis was used to quantitate the cartilage callus volume / total callus volume (CV/TV) or bony callus volume / total callus volume (BV/TV). Results X-ray exam-ination revealed that on the 21st day after fracture, callus appeared at the fracture gap to form a bony bridge in WT mice while a radiolucent zone was apparent in the fracture gap in the Col2al-ICAT transgenic mice. Histology observation revealed that compared with WT mice, the formation of cartilage callus and endochondral ossification were delayed in Col2al-ICAT transgenic mice. Histomorphometric analysis indicated that the peak value of CV/TV arrived later in Col2al-ICAT transgenie mice than in WT mice. The BV/TV in Col2al-ICAT transgenic mice was significantly less than that in WT mice on 14th and 21st days after fracture (P<0.05). Conclusion The Wnt/β-catenin signals cause delayed fracture healing in Col2al-ICAT transgenic mice by affecting the cartilage callus formation and endochondral ossification. Key words: Wnt/β-catenin; Signal transduction; Osteogenesis; Fracture healing; Molecular mechanism of action
Published Version
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