Bone fracture in a rat femoral fracture model is associated with the activation of autophagy.

ABSTRACT

Autophagy, which is a mechanism for the turnover of intracellular molecules and organelles, protects cells during stress responses; however, the role of autophagy in the stages of bone fracture remains to be elucidated. The aim of the present study was to investigate the process of autophagy in bone tissue at different time-points after fracture. A femur fracture model was established in male adult Wistar rats via surgery. The protein expression of microtubule-associated protein II light chain 3 (LC3-II) was analyzed in a femur fracture (experimental) group and a sham-surgery group using immunofluorescence. The protein expression of proliferating cell nuclear antigen (PCNA) was used to investigate the cell proliferation in bone tissue following fracture via immunohistochemical analysis. The correlation between cell proliferation and autophagy was analyzed using linear regression. LC3-II protein was constitutively expressed in the sham-surgery group; however, compared with the expression in the sham-surgery group, the LC3-II expression in the experimental group was significantly increased at each time-point (P<0.05). Similarly, immunohistochemistry revealed that the number of PCNA-positive cells in each section was significantly increased following fracture injury (P<0.01). A comparison of the LC3-II- and PCNA-positive rates in the experimental group rats at each time-point revealed a linear correlation (R2=0.43, P<0.01). In conclusion, surgically induced fracture in rats is associated with an increase in LC3-II and PCNA protein expression during the initial stages of fracture injury, and a correlation exists between the expression of the two proteins. These results suggest that potential treatment aimed at improving fracture healing should target the process of autophagy.