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Beneficial role of microRNA-328-3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway
Although fragility fracture is a global public health burden, the mechanisms underlying fracture healing remain unclear. The present study aimed to assess the dynamic expression pattern of microRNA-328-3p (miR-328-3p) during fracture healing in patients with fragility fracture and to explore the fun...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7664617/ https://www.ncbi.nlm.nih.gov/pubmed/33199996 http://dx.doi.org/10.3892/etm.2020.9401 |
Sumario: | Although fragility fracture is a global public health burden, the mechanisms underlying fracture healing remain unclear. The present study aimed to assess the dynamic expression pattern of microRNA-328-3p (miR-328-3p) during fracture healing in patients with fragility fracture and to explore the functional role and mechanisms of miR-328-3p in the regulation of osteoblastic viability. The expression levels of miR-328-3p was examined using reverse transcription-quantitative PCR (RT-qPCR). Osteoblastic proliferation and apoptosis were analyzed via MTT and flow cytometry assays. A luciferase reporter assay was adopted to confirm the interaction between miR-328-3p and its target gene PTEN, and western blotting was used to explore the activity of PI3K/AKT signaling. The results of the present study demonstrated that serum miR-328-3p expression did not significantly differ at the early stage of healing in patients with fracture, but was markedly decreased 14 and 21 days post fixation (P<0.01). PTEN was demonstrated to be a target gene of miR-328-3p and was inhibited by miR-328-3p overexpression in osteoblasts (P<0.001). miR-328-3p overexpression increased osteoblastic proliferation but decreased apoptotic rate, with these effects being reversed by PTEN overexpression (P<0.05). The expression of phosphorylated-AKT was elevated in osteoblasts by miR-328-3p overexpression, but this effect was abolished by overexpressing PTEN. Thus, the present study revealed that miR-328-3p may accelerate fracture healing by promoting osteoblastic viability through the PTEN/PI3K/AKT pathway. |
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