Beneficial role of microRNA‑328‑3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway
- Wei Xie
- Zhuqing Wang
- Yanbo Zhang
- Zhenpeng Zhang
Affiliations: Department of Sport Medicine, Traditional Chinese Medicine Hospital of Weifang, Weifang, Shandong 261041, P.R. China
- Published online on: October 27, 2020 https://doi.org/10.3892/etm.2020.9401
Copyright: © Xie
et al. This is an open access article distributed under the
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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.