The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/phosphoinositide 3-kinase signaling pathway

Background The underlying mechanism of micro (mi)RNA-211 in bone cell apoptosis after fracture remains unclear. This study aimed to determine the effect and function of miRNA-211 in bone cell apoptosis in fracture patients. Methods Serum samples were collected from patients with fractures and healthy controls. Serum miR-211 expression was detected by quantitative PCR. MC3T3-E1 cells were transfected with a transforming growth factor (TGF)-beta inhibitor and phosphoinositide 3-kinase (PI3K) inhibitor. The viability of MC3T3-E1 cells was detected by the MTT assay, and apoptosis was detected by flow cytometry. Caspase-3/9 activity and the protein expression of TGF-beta, PI3K, and p-Akt were detected by western blot and immunoprecipitation. Results In the fracture group, miRNA-211 expression was significantly up-regulated compared with controls. We used miRNA-211 mimics to up-regulate miRNA-211 expression, and observed inhibited cell viability and induced apoptosis and lactate dehydrogenase (LDH) activity. miRNA-211 up-regulation also suppressed the expression of TGF-beta, PI3K, and p-Akt proteins. Conversely, miRNA-211 down-regulation increased cell viability and reduced apoptosis and LDH activity, as well as inducing the expression of TGF-beta, PI3K, and p-Akt. Inhibiting TGF-beta decreased the effect of anti-miRNA-211 on osteocyte apoptosis. Conclusion Our data indicate that miRNA-211 functions via the TGF-beta/PI3K/Akt signaling pathway in patients with fractures.