MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2
| Autor: | Ke Xu, Haihao Wu, Bin Wang, Wei Wu |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Male
Cell Survival Apoptosis Bioengineering Bone healing Applied Microbiology and Biotechnology Cell Line Flow cytometry Fractures Bone Mice microRNA medicine Animals Humans Viability assay Receptor Fibroblast Growth Factor Type 2 Fracture Healing Osteoblasts Base Sequence medicine.diagnostic_test Chemistry Fibroblast growth factor receptor 2 fgfr2 General Medicine Transfection Middle Aged MicroRNAs Real-time polymerase chain reaction Gene Expression Regulation Cancer research Female Mir-223-3p TP248.13-248.65 Research Article Research Paper Biotechnology |
| Zdroj: | Bioengineered article-version (VoR) Version of Record Bioengineered, Vol 12, Iss 2, Pp 12040-12048 (2021) |
| ISSN: | 2165-5987 2165-5979 |
| Popis: | MicroRNAs (miRNAs) are powerful modulators of fracture healing. The research explored the level of serum miR-223-3p in fracture patients and its potential mechanism in fracture healing. In the study, miR-223-3p levels in 42 patients with intra-articular fracture and 40 patients with hand fracture were detected by real-time fluorescence quantitative PCR reaction (qRT-PCR). Subsequently, osteoblasts MC3T3-E1 was transfected with miR-223-3p mimic or inhibitor, and cell function was detected by Cell counting kit (CCK-8) assay and flow cytometry. Dual-luciferase reporter assay verified the regulation mechanism of miR-223-3p and its target genes. We found that miR-223-3p was significantly elevated over time in patients with intra-articular fracture and hand fracture compared with healthy individuals. Moreover, increased miR-223-3p significantly reduced cell viability and promoted cell apoptosis. The fibroblast growth factor receptor 2 (FGFR2) was the target of miR-223-3p. Serum FGFR2 was significantly decreased in patients, which was contrary to the expression of miR-223-3p. Moreover, FGFR2 levels in cells were negatively regulated by miR-223-3p. Finally, si-FGFR2 significantly reversed the promotion of miR-223-3p inhibitor on cell viability and the inhibition of cell apoptosis. Our research suggested that miR-223-3p is highly expressed in fracture patients, and regulates osteoblast cell viability and apoptosis by targeting FGFR2. This may be a valuable target for fracture healing therapy and provide a new perspective for its treatment. |
| Databáze: | OpenAIRE |
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