MiR-133a inhibits fracture healing via targeting RUNX2/BMP2

To analyze the mechanism of miR-133a in inhibiting fracture healing through regulating runt-related transcription factor 2 (RUNX2) signaling pathway.

A total of 80 patients with fracture admitted to our hospital from January 2016 to January 2017 were divided into 2 groups according to nonunion fracture or healing fracture: nonunion fracture group (n = 40) and control group (n= 40). After admission, patients underwent the surgery, respectively, and the bone tissues were taken for stand-by application. The expression level of bone morphogenetic protein 2 (BMP2) was detected using the immunohistochemical method, the expression level of RUNX2 protein was detected by Western blotting, and the expression level of micro ribonucleic acid (miR)-133a was detected by quantitative polymerase chain reaction (qPCR). Moreover, the bioinformatics method was used to predict the target gene of miR-133a, and the luciferase reporter gene was used to detect the binding of miR-133a to RUNX2.

Compared with those in control group, the expression of BMP2 and the relative expressions of RUNX2 protein and miR-133a were significantly decreased; the differences were statistically significant (p < 0.05). Pearson correlation analysis showed that miR-133a was negatively correlated with RUNX2. After overexpression of miR-133a, the expression level of RUNX2 was decreased, but it was increased significantly after interference in miR-133a. Besides, it was found in dual-luciferase reporter assay that miR-133a bound to RUNX2.

MiR-133a inhibits the bone formation through inhibiting the RUNX2/BMP2 signaling pathway, thereby negatively regulating the fracture healing.