Regulatory Effect of miR-92b-3p on Delayed Healing of Tibial Fractures

Delayed fracture healing (DFH) prolongs hospital stays and intensifies patients' discomfort, seriously affecting their quality of life. The present study was designed to elucidate the function of miR-92b-3p in fracture healing and evaluate the diagnostic value of serum miR-92b-3p for DFH. This study included 260 patients with tibial fractures: 196 with normal fracture healing (NFH) and 64 with DFH. Serum miR-92b-3p level was measured by RT-qPCR. The diagnostic potential of miR-92b-3p for DFH was evaluated by the Receiver operating characteristic (ROC) curve. MiR-92b-3p was overexpressed or inhibited in hFOB 1.19 cells by cell transfection. Osteogenic differentiation of hFOB 1.19 cells was induced using osteogenic medium. Then, the levels of bone formation markers were detected by RT-qPCR. Serum miR-92b-3p levels were reduced in DFH and showed high diagnostic potential. MiR-92b-3p level was related to diabetes in patients with DFH. In addition, miR-92b-3p was a risk factor for DFH. During osteogenic differentiation, miR-92b-3p levels increased. On the 14th day of osteogenic differentiation, overexpression of miR-92b-3p elevated proliferation and the levels of bone formation markers, while inhibition of miR-92b-3p reduced proliferation and the levels of bone formation markers. phosphatase and tensin homolog (PTEN) was identified as a downstream target gene of miR-92b-3p using the ENCORI database, and its interaction was validated by dual-luciferase reporter assay, with PTEN overexpression reversing the miR-92b-3p mimic-induced upregulation of bone formation marker levels. MiR-92b-3p may participate in DFH by regulating proliferation and bone formation markers, and it may serve as a biomarker for DFH.