Identification of miRNA Regulatory Networks and Candidate Markers for Fracture Healing in Mice

Li, Xianglu; Zhong, Zhaohua; Ma, Enguang; Wu, Xiaowei

doi:10.1155/2021/2866475

Cited by 5 publications

(3 citation statements)

References 26 publications

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“…Inhibitory miRNAs can inhibit osteoblast CP and promote CA by targeting osteogenic genes in vitro [7,8]. For example, increased miR-221-3p expression during bone healing in diabetic fracture patients can lead to impaired endochondral ossification and reduced bone remodeling [9].…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Downregulation of miR‐221‐3p by LncRNA TUG1 Promoting the Healing of Closed Tibial Fractures in Mice

Liu

Yuan

2022

BioMed Research International

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Objective. To probe into the effect of LncRNA TUG1 on the healing of closed tibial fracture in mice. Methods. The closed tibial fracture model of mice was established, selecting the mouse osteoblast line MC3T3-E1, with the cells separated into four groups. The expression levels of TUG1 and miR-221-3p were determined by RT-qPCR analysis, with the targeting relationship between TUG1 and miR-221-3p authenticated by dual luciferase reporter (DLR) assay, detection of cell migration (CM) ability based on Transwell cell migration (TCM) assay, and cell proliferation (CP) acquired by cell counting kit-8 (CCK-8). Results. Prediction results of the target gene by bioinformatics software showed that miR-221-3p had binding sites with the 3 ′ -UTR of TUG1, and DLR assay authenticated the targeting relationship between LncRNA TUG1 and miR-221-3p. Downregulation of TUG1 inhibited osteoblast CP and CM and promoted osteoblast cell apoptosis (CA). Cell cycle analysis indicated that miR-221-3p provoked cell cycle arrest in G1 stage of MC3T3-E1 cells. The siLncRNA-NC group had higher anticyclin D1 and D3 levels than the siLncRNA TUG1 group, with a lower CA rate in the former, implying that miR-221-3p overexpression inhibited osteoblast CP and CM and LncRNA TUG1 inhibited CA. Downregulation of miR-221-3p partly reversed the retardation out of downregulating TUG1 on osteoblast CP and CM. Bcl-2 level was higher in the LncRNA TUG1 group compared to the siLncRNA TUG1 and miR-221-3p overexpression groups, with remarkably lower SDF-1 level in the miR-221-3p overexpression group than those in the control, miRNA-NC, and LncRNA TUG1 groups. Conclusion. The downregulation of miR-221-3p by LncRNA TUG1 can promote the healing of closed tibial fractures in mice.

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Section: Introductionmentioning

confidence: 99%

[Retracted] Downregulation of miR‐221‐3p by LncRNA TUG1 Promoting the Healing of Closed Tibial Fractures in Mice

Liu

Yuan

2022

BioMed Research International

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“…Plasma miR-92a plays an important role in human fracture healing, and its inhibition promotes fracture healing through angiogenesis ( Murata et al, 2014 ). It has also been shown that the miRNA–mRNA network has a regulatory role in osteoblast differentiation, the pathogenesis of osteoporosis, and fracture healing ( An et al, 2014 ; Zhang et al, 2020 ; Li et al, 2021 ; Mohanapriya et al, 2022 ). Based on the advantages of miRNA, transcriptome analysis combining miRNA and mRNA of fractures will help to identify potential therapeutic targets for fracture healing.…”

Section: Introductionmentioning

confidence: 99%

Identification of the miRNA–mRNA regulatory network in a mouse model of early fracture

Wang,

Xie,

Yan

et al. 2024

Front. Genet.

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Fracture healing is a complex process that involves multiple molecular events, and the regulation mechanism is not fully understood. We acquired miRNA and mRNA transcriptomes of mouse fractures from the Gene Expression Omnibus database (GSE76197 and GSE192542) and integrated the miRNAs and genes that were differentially expressed in the control and fracture groups to construct regulatory networks. There were 130 differentially expressed miRNAs and 4,819 differentially expressed genes, including 72 upregulated and 58 downregulated miRNAs, along with 2,855 upregulated and 1964 downregulated genes during early fracture healing. Gene ontology analysis revealed that most of the differentially expressed genes were enriched in the extracellular matrix (ECM) structure and the ECM organization. The Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment suggested cell cycle, DNA replication, and mismatch repair were involved in the progression of fracture healing. Furthermore, we constructed a molecular network of miRNAs and mRNAs with inverse expression patterns to elucidate the molecular basis of miRNA–mRNA regulation in fractures. The regulatory network highlighted the potential targets, which may help to provide a mechanistic basis for therapies to improve fracture patient outcomes.

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“…Plasma miR-92a plays an important role in human fracture healing, and its inhibition promotes fracture healing through angiogenesis (Murata et al, 2014). It has also been shown that the miRNA-mRNA network has a regulatory role in osteoblast differentiation, the pathogenesis of osteoporosis, and fracture healing (An et al, 2014;Zhang et al, 2020;Li et al, 2021;Mohanapriya et al, 2022). Based on the advantages of miRNA, transcriptome analysis combining miRNA and mRNA of fractures will help to identify potential therapeutic targets for fracture healing.…”

Section: Introductionmentioning

confidence: 99%

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Identification of miRNA Regulatory Networks and Candidate Markers for Fracture Healing in Mice

Cited by 5 publications

References 26 publications

[Retracted] Downregulation of miR‐221‐3p by LncRNA TUG1 Promoting the Healing of Closed Tibial Fractures in Mice

[Retracted] Downregulation of miR‐221‐3p by LncRNA TUG1 Promoting the Healing of Closed Tibial Fractures in Mice

Identification of the miRNA–mRNA regulatory network in a mouse model of early fracture

Table2.xlsx

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