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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)-β 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-β, 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-β, 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-β, PI3K, and p-Akt. Inhibiting TGF-β decreased the effect of anti-miRNA-211 on osteocyte apoptosis. Conclusion Our data indicate that miRNA-211 functions via the TGF-β/PI3K/Akt signaling pathway in patients with fractures.

A computer-aided semantic analysis (using Linguistic Inquiry and Word Count [LIWC]) examined how newspaper coverage of air pollution from 2014 to 2017 may affect the public agenda in four cities—Hong Kong, London, Pittsburgh, and Tianjin. Results show that after controlling for the real-time air quality, the agenda-setting effect was found in Hong Kong, London, and Pittsburgh, but not Tianjin. Tianjin’s reports also contained more future-framed words but fewer present-framed words than other cities.