The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/ phosphoinositide 3-kinase signaling pathway
Background The underlying mechanism of micro (mi)RNA-211 in bone cell apoptosis after fracture remains unclear. This study aimed to determine the effect and function of miRNA-211 in bone cell apoptosis in fracture patients. Methods Serum samples were collected from patients with fractures and health...
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Format: | Article |
Language: | English |
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SAGE Publishing
2020-07-01
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Series: | Journal of International Medical Research |
Online Access: | https://doi.org/10.1177/0300060520926353 |
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author | Tongxin Sun Dai Yang Yuanpeng Wu Qingang Sheng |
author_facet | Tongxin Sun Dai Yang Yuanpeng Wu Qingang Sheng |
author_sort | Tongxin Sun |
collection | DOAJ |
description | Background The underlying mechanism of micro (mi)RNA-211 in bone cell apoptosis after fracture remains unclear. This study aimed to determine the effect and function of miRNA-211 in bone cell apoptosis in fracture patients. Methods Serum samples were collected from patients with fractures and healthy controls. Serum miR-211 expression was detected by quantitative PCR. MC3T3-E1 cells were transfected with a transforming growth factor (TGF)-β inhibitor and phosphoinositide 3-kinase (PI3K) inhibitor. The viability of MC3T3-E1 cells was detected by the MTT assay, and apoptosis was detected by flow cytometry. Caspase-3/9 activity and the protein expression of TGF-β, PI3K, and p-Akt were detected by western blot and immunoprecipitation. Results In the fracture group, miRNA-211 expression was significantly up-regulated compared with controls. We used miRNA-211 mimics to up-regulate miRNA-211 expression, and observed inhibited cell viability and induced apoptosis and lactate dehydrogenase (LDH) activity. miRNA-211 up-regulation also suppressed the expression of TGF-β, PI3K, and p-Akt proteins. Conversely, miRNA-211 down-regulation increased cell viability and reduced apoptosis and LDH activity, as well as inducing the expression of TGF-β, PI3K, and p-Akt. Inhibiting TGF-β decreased the effect of anti-miRNA-211 on osteocyte apoptosis. Conclusion Our data indicate that miRNA-211 functions via the TGF-β/PI3K/Akt signaling pathway in patients with fractures. |
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institution | Directory Open Access Journal |
issn | 1473-2300 |
language | English |
last_indexed | 2024-12-20T06:02:00Z |
publishDate | 2020-07-01 |
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series | Journal of International Medical Research |
spelling | doaj.art-e832a873ff3f47a29b09b918157d2b872022-12-21T19:50:53ZengSAGE PublishingJournal of International Medical Research1473-23002020-07-014810.1177/0300060520926353The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/ phosphoinositide 3-kinase signaling pathwayTongxin SunDai YangYuanpeng WuQingang ShengBackground The underlying mechanism of micro (mi)RNA-211 in bone cell apoptosis after fracture remains unclear. This study aimed to determine the effect and function of miRNA-211 in bone cell apoptosis in fracture patients. Methods Serum samples were collected from patients with fractures and healthy controls. Serum miR-211 expression was detected by quantitative PCR. MC3T3-E1 cells were transfected with a transforming growth factor (TGF)-β inhibitor and phosphoinositide 3-kinase (PI3K) inhibitor. The viability of MC3T3-E1 cells was detected by the MTT assay, and apoptosis was detected by flow cytometry. Caspase-3/9 activity and the protein expression of TGF-β, PI3K, and p-Akt were detected by western blot and immunoprecipitation. Results In the fracture group, miRNA-211 expression was significantly up-regulated compared with controls. We used miRNA-211 mimics to up-regulate miRNA-211 expression, and observed inhibited cell viability and induced apoptosis and lactate dehydrogenase (LDH) activity. miRNA-211 up-regulation also suppressed the expression of TGF-β, PI3K, and p-Akt proteins. Conversely, miRNA-211 down-regulation increased cell viability and reduced apoptosis and LDH activity, as well as inducing the expression of TGF-β, PI3K, and p-Akt. Inhibiting TGF-β decreased the effect of anti-miRNA-211 on osteocyte apoptosis. Conclusion Our data indicate that miRNA-211 functions via the TGF-β/PI3K/Akt signaling pathway in patients with fractures.https://doi.org/10.1177/0300060520926353 |
spellingShingle | Tongxin Sun Dai Yang Yuanpeng Wu Qingang Sheng The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/ phosphoinositide 3-kinase signaling pathway Journal of International Medical Research |
title | The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/ phosphoinositide 3-kinase signaling pathway |
title_full | The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/ phosphoinositide 3-kinase signaling pathway |
title_fullStr | The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/ phosphoinositide 3-kinase signaling pathway |
title_full_unstemmed | The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/ phosphoinositide 3-kinase signaling pathway |
title_short | The function of microRNA-211 expression in post-fracture bone cell apoptosis involving the transforming growth factor-β/ phosphoinositide 3-kinase signaling pathway |
title_sort | function of microrna 211 expression in post fracture bone cell apoptosis involving the transforming growth factor β phosphoinositide 3 kinase signaling pathway |
url | https://doi.org/10.1177/0300060520926353 |
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