MiR-214-3p delays fracture healing in rats with osteoporotic fracture through inhibiting BMP/Smad signaling pathway

The purpose of this study was to explore the mechanism of micro-ribonucleic acid (miR)-214-3p in regulating fracture healing in rats with osteoporosis.A total of 30 female Sprague-Dawley rats were selected and randomly divided into 3 groups, including group A [phosphate-buffered saline (PBS), n=10], group B (AntagomiR-NC, n=10), and group C (AntagomiR-214-3p, n=10). All rats underwent ovariectomy, and the osteoporosis rat model was verified by dual-energy X-ray absorptiometry 8 weeks after the operation. Then the osteoporotic fracture was established in rats via a second operation. From the successful modeling until the 6th week, 50 μL PBS (2 nmoL) was intraperitoneally injected in group A, an equal amount of AntagomiR-NC was injected in group B, and an equal amount of AntagomiR-214-3p was injected in group C once a week. At the 6th week, fracture healing of osteoporosis rats was evaluated. At the same time, the expression of miR-214-3p in the three groups was detected via reverse Transcription-Polymerase Chain Reaction (RT-PCR). Furthermore, the protein expressions of bone morphogenetic protein 2 (BMP2) and Smad4 in the three groups were detected via Western blotting (WB).After ovariectomy, the bone mineral density in each group was significantly lower than that before ovariectomy, and the differences were statistically significant (p0.05). Imaging evaluation demonstrated that compared with group A and B, there were significantly more callus tissues in group C. Meanwhile, the fracture line healing was better and blurred, and the internal fixation had no displacement and loosening. RT-PCR results indicated that the expression level of miR-214-3p in group C was significantly lower than that of the other two groups (p0.05). WB results showed that the protein expression levels of BMP2 and Smad4 in group C were significantly higher than those of group A and group B (p0.05).MiR-214-3p delays fracture healing in rats with osteoporotic fracture by inhibiting the BMP/Smad signaling pathway.