Functional Mechanism and Clinical Implications of miR-378a-3p in Femoral Shaft Fracture Healing Processes.

Femoral shaft fractures are high-energy injuries to the femur that have a probability of delayed union. Prolonged fracture healing time can cause more pain and financial burden to the patient. miR-378a-3p has been reported to be the promoter of bone formation. This study thus investigated the association between miR-378a-3p and femoral shaft fracture delayed union, as well as the underlying mechanism. This study aimed to provide valuable information on treating femoral shaft fracture and preventing its delayed union. Serum samples were obtained from femoral shaft fracture delayed or normal-union patients to investigate the expression level of miR-378a-3p. Cell experiments were conducted using the MC3T3-E1 cell line to explore the underlying mechanism. The quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of microRNA (miRNA) and gene. To estimate the effect of miR-378a-3p and Zinc Finger Protein, FOG Family Member 2 (ZFPM2) on osteoblast proliferation, Cell Counting Kit-8 (CCK-8) was chosen in this study. The mechanism was investigated using dual luciferase reporter assay. miR-378a-3p was downregulated in femoral shaft fracture patients with delayed union. The miR-378a-3p downregulation was found as an independent risk factor for the delayed union of femoral shaft fracture. miR-378a-3p could facilitate osteoblast proliferation and differentiation. miR-378a-3p affected osteoblast activities by targeting ZFPM2. In conclusion, the miR-378a-3p downregulation was an indicator of delayed union of femoral shaft fracture. miR-378a-3p played a crucial role in the fracture healing process. ZFPM2 mediated the effect of miR-378a-3p on the fracture healing process.