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...

Full description

Bibliographic Details
Main Authors: Tongxin Sun, Dai Yang, Yuanpeng Wu, Qingang Sheng
Format: Article
Language:English
Published: SAGE Publishing 2020-07-01
Series:Journal of International Medical Research
Online Access:https://doi.org/10.1177/0300060520926353
_version_ 1818938070155657216
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.
first_indexed 2024-12-20T06:02:00Z
format Article
id doaj.art-e832a873ff3f47a29b09b918157d2b87
institution Directory Open Access Journal
issn 1473-2300
language English
last_indexed 2024-12-20T06:02:00Z
publishDate 2020-07-01
publisher SAGE Publishing
record_format Article
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
work_keys_str_mv AT tongxinsun thefunctionofmicrorna211expressioninpostfracturebonecellapoptosisinvolvingthetransforminggrowthfactorbphosphoinositide3kinasesignalingpathway
AT daiyang thefunctionofmicrorna211expressioninpostfracturebonecellapoptosisinvolvingthetransforminggrowthfactorbphosphoinositide3kinasesignalingpathway
AT yuanpengwu thefunctionofmicrorna211expressioninpostfracturebonecellapoptosisinvolvingthetransforminggrowthfactorbphosphoinositide3kinasesignalingpathway
AT qingangsheng thefunctionofmicrorna211expressioninpostfracturebonecellapoptosisinvolvingthetransforminggrowthfactorbphosphoinositide3kinasesignalingpathway
AT tongxinsun functionofmicrorna211expressioninpostfracturebonecellapoptosisinvolvingthetransforminggrowthfactorbphosphoinositide3kinasesignalingpathway
AT daiyang functionofmicrorna211expressioninpostfracturebonecellapoptosisinvolvingthetransforminggrowthfactorbphosphoinositide3kinasesignalingpathway
AT yuanpengwu functionofmicrorna211expressioninpostfracturebonecellapoptosisinvolvingthetransforminggrowthfactorbphosphoinositide3kinasesignalingpathway
AT qingangsheng functionofmicrorna211expressioninpostfracturebonecellapoptosisinvolvingthetransforminggrowthfactorbphosphoinositide3kinasesignalingpathway