期刊
JOURNAL OF INTERNATIONAL MEDICAL RESEARCH
卷 48, 期 7, 页码 -出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/0300060520926353
关键词
MicroRNA-211; fracture; transforming growth factor-beta; phosphoinositide 3-kinase/Akt; bone cell apoptosis; osteocytes; osteoporosis
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.
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