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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 |
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author | Xie, Wei Wang, Zhuqing Zhang, Yanbo Zhang, Zhenpeng |
author_facet | Xie, Wei Wang, Zhuqing Zhang, Yanbo Zhang, Zhenpeng |
author_sort | Xie, Wei |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7664617 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-76646172020-11-15 Beneficial role of microRNA-328-3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway Xie, Wei Wang, Zhuqing Zhang, Yanbo Zhang, Zhenpeng Exp Ther Med Articles 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. D.A. Spandidos 2020-12 2020-10-27 /pmc/articles/PMC7664617/ /pubmed/33199996 http://dx.doi.org/10.3892/etm.2020.9401 Text en Copyright: © Xie et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Xie, Wei Wang, Zhuqing Zhang, Yanbo Zhang, Zhenpeng Beneficial role of microRNA-328-3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway |
title | Beneficial role of microRNA-328-3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway |
title_full | Beneficial role of microRNA-328-3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway |
title_fullStr | Beneficial role of microRNA-328-3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway |
title_full_unstemmed | Beneficial role of microRNA-328-3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway |
title_short | Beneficial role of microRNA-328-3p in fracture healing by enhancing osteoblastic viability through the PTEN/PI3K/AKT pathway |
title_sort | beneficial role of microrna-328-3p in fracture healing by enhancing osteoblastic viability through the pten/pi3k/akt pathway |
topic | Articles |
url | 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 |
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