LncRNA MIR22HG promotes fracture healing through down-regulation of miR-10a-5p

Delayed fracture healing (DFH) is a common postoperative complication in fractured patients, impairing affects quality of life and increasing financial burden.

This study explored the clinical significance of long noncoding RNA (lncRNA) MIR22HG in DFH and its potential mechanisms in promoting fracture healing.

A total of 145 patients with normal healing and 132 patients with DFH were enrolled. Quantitative PCR was used to detect the expression levels of MIR22HG, miR-10a-5p, and osteogenic differentiation-related genes. ROC curves and logistic analysis were performed to evaluate the predictive value of MIR22HG. Using the hFOB 1.19 osteogenic differentiation model, the effects of MIR22HG silencing and co-inhibition of MIR22HG and miR-10a-5p on osteogenic differentiation were explored, and the proliferation and apoptosis were detected via CCK-8 assay and flow cytometry.

Serum MIR22HG were decreased, while miR-10a-5p was elevated in DFH patients. MIR22HG could distinguish DFH patients and predict DFH occurrence. In the hFOB 1.19 osteogenic differentiation model, silencing MIR22HG reduced the expression of osteogenic differentiation markers, inhibited cell proliferation and promoted apoptosis. MIR22HG negatively regulated miR-10a-5p, and miR-10a-5p effectively reversed the inhibitory effect of MIR22HG silencing on hFOB 1.19 cell function.

MIR22HG promotes fracture healing by sponging miR-10a-5p. Serum MIR22HG is a potential marker for the clinically assisted prediction of DFH occurrence. MIR22HG/miR-10a-5p axis provides a potential molecular target for fracture healing treatment.