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Beneficial role of microRNA‑328‑3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway
Author(s) -
Wei Xie,
Zhuqing Wang,
Yanbo Zhang,
Zhenpeng Zhang
Publication year - 2020
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2020.9401
Subject(s) - pten , pi3k/akt/mtor pathway , protein kinase b , bone healing , microrna , cancer research , viability assay , apoptosis , osteoblast , mtt assay , signal transduction , microbiology and biotechnology , biology , chemistry , gene , anatomy , biochemistry , in vitro
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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