MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2

MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2

MicroRNAs (miRNAs) are powerful modulators of fracture healing. The research explored the level of serum miR-223-3p in fracture patients and its potential mechanism in fracture healing. In the study, miR-223-3p levels in 42 patients with intra-articular fracture and 40 patients with hand fracture we...

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Autores principales: Bin Wang, Wei Wu, Ke Xu, Haihao Wu
Formato: article
Lenguaje:EN
Publicado: Taylor & Francis Group 2021
Materias:
mir-223-3p
fracture healing
fgfr2
Biotechnology
TP248.13-248.65
Acceso en línea:https://doaj.org/article/54835da3e6a0465b84eb717c0bebc027
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spelling oai:doaj.org-article:54835da3e6a0465b84eb717c0bebc0272021-11-11T14:23:43ZMicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 22165-59792165-598710.1080/21655979.2021.2002498https://doaj.org/article/54835da3e6a0465b84eb717c0bebc0272021-11-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.2002498https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987MicroRNAs (miRNAs) are powerful modulators of fracture healing. The research explored the level of serum miR-223-3p in fracture patients and its potential mechanism in fracture healing. In the study, miR-223-3p levels in 42 patients with intra-articular fracture and 40 patients with hand fracture were detected by real-time fluorescence quantitative PCR reaction (qRT-PCR). Subsequently, osteoblasts MC3T3-E1 was transfected with miR-223-3p mimic or inhibitor, and cell function was detected by Cell counting kit (CCK-8) assay and flow cytometry. Dual-luciferase reporter assay verified the regulation mechanism of miR-223-3p and its target genes. We found that miR-223-3p was significantly elevated over time in patients with intra-articular fracture and hand fracture patients compared with healthy individuals. Moreover, increased miR-223-3p significantly reduced cell viability and promoted cell apoptosis. The fibroblast growth factor receptor 2 (FGFR2) was the target of miR-223-3p. Serum FGFR2 was significantly decreased in patients, which was contrary to the expression of miR-223-3p. Moreover, FGFR2 levels in cells were negatively regulated by miR-223-3p. Finally, si-FGFR2 significantly reversed the promotion of miR-223-3p inhibitor on cell viability and the inhibition of cell apoptosis. Our research suggested that miR-223-3p is highly expressed in fracture patients, and regulates osteoblast cell viability and apoptosis by targeting FGFR2. This may be a valuable target for fracture healing therapy and provide a new perspective for its treatment.Bin WangWei WuKe XuHaihao WuTaylor & Francis Grouparticlemir-223-3pfracture healingfgfr2BiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution DOAJ
collection DOAJ
language EN
topic mir-223-3p
fracture healing
fgfr2
Biotechnology
TP248.13-248.65
spellingShingle mir-223-3p
fracture healing
fgfr2
Biotechnology
TP248.13-248.65
Bin Wang
Wei Wu
Ke Xu
Haihao Wu
MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2
description MicroRNAs (miRNAs) are powerful modulators of fracture healing. The research explored the level of serum miR-223-3p in fracture patients and its potential mechanism in fracture healing. In the study, miR-223-3p levels in 42 patients with intra-articular fracture and 40 patients with hand fracture were detected by real-time fluorescence quantitative PCR reaction (qRT-PCR). Subsequently, osteoblasts MC3T3-E1 was transfected with miR-223-3p mimic or inhibitor, and cell function was detected by Cell counting kit (CCK-8) assay and flow cytometry. Dual-luciferase reporter assay verified the regulation mechanism of miR-223-3p and its target genes. We found that miR-223-3p was significantly elevated over time in patients with intra-articular fracture and hand fracture patients compared with healthy individuals. Moreover, increased miR-223-3p significantly reduced cell viability and promoted cell apoptosis. The fibroblast growth factor receptor 2 (FGFR2) was the target of miR-223-3p. Serum FGFR2 was significantly decreased in patients, which was contrary to the expression of miR-223-3p. Moreover, FGFR2 levels in cells were negatively regulated by miR-223-3p. Finally, si-FGFR2 significantly reversed the promotion of miR-223-3p inhibitor on cell viability and the inhibition of cell apoptosis. Our research suggested that miR-223-3p is highly expressed in fracture patients, and regulates osteoblast cell viability and apoptosis by targeting FGFR2. This may be a valuable target for fracture healing therapy and provide a new perspective for its treatment.
format article
author Bin Wang
Wei Wu
Ke Xu
Haihao Wu
author_facet Bin Wang
Wei Wu
Ke Xu
Haihao Wu
author_sort Bin Wang
title MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2
title_short MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2
title_full MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2
title_fullStr MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2
title_full_unstemmed MicroRNA-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2
title_sort microrna-223-3p is involved in fracture healing by regulating fibroblast growth factor receptor 2
publisher Taylor & Francis Group
publishDate 2021
url https://doaj.org/article/54835da3e6a0465b84eb717c0bebc027
work_keys_str_mv AT binwang microrna2233pisinvolvedinfracturehealingbyregulatingfibroblastgrowthfactorreceptor2
AT weiwu microrna2233pisinvolvedinfracturehealingbyregulatingfibroblastgrowthfactorreceptor2
AT kexu microrna2233pisinvolvedinfracturehealingbyregulatingfibroblastgrowthfactorreceptor2
AT haihaowu microrna2233pisinvolvedinfracturehealingbyregulatingfibroblastgrowthfactorreceptor2
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