miR-3065-5p regulates mouse odontoblastic differentiation partially through bone morphogenetic protein receptor type II

Lin, Chujiao; Zhang, Qian; Yu, Shuaitong; Lin, Yuxiu; Li, Shu-Chen; Liu, Huan; Chen, Zhi

doi:10.1016/j.bbrc.2017.11.026

Cited by 9 publications

(8 citation statements)

References 22 publications

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“…It was reported that miR-3065 was related to odontoblastic differentiation and postmenopausal osteoporosis. 21,22 Moreover, we found that BC049715-OT4, Lmf2-206, Snx24-OT3, and 2010111I01Rik-AS1 may function as ceRNAs to suppress the inhibitory effects of mus-miR-3065-3p on Myo18a, which is closely involved in suppressing inflammatory responsiveness of macrophages via a mechanism that modulates CD14 trafficking. 23 Accumulating studies have shown that circRNAs play roles as a miRNA sponge by competitively binding MRE.…”

Section: Construction Of Co-expression Networkmentioning

confidence: 87%

Integrative analyses reveal RNA regulatory network in Ti particles induced inflammation

Jiang

Zhang

et al. 2021

Eur J Inflamm

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Introduction Wear particles induced inflammatory osteolysis is the most important initiating factors in the mechanism of aseptic loosening. However, the molecular network changes in this process remain largely elusive. Methods Here, we performed whole transcriptome analysis using Ti particles induced RAW264.7 cell model to identify specific genes and pathways. Results Sequencing results totally identified 159 mRNAs, 96 lncRNAs, 31 circRNAs, and 12 miRNAs were significantly differently expressed. Of these, we selected two of each RNA for qRT-PCR validation and the results were highly consistent with the RNA-seq data. GSEA analysis shows that upregulated gene sets were related to the three classical inflammation pathway, cytokine–cytokine receptor interaction, TNF, and NF-kappa B signaling pathway. The enriched genes included not only IL-1β and TNF- α, which were independently verified before sequencing, but also other inflammatory osteolysis-related genes such as Mmp9, Fas, and Ccl2. Co-differentially expressed RNAs were employed to construct the ceRNA co-regulatory network. Conclusion: The results revealed that 4 lncRNAs and 2 circRNAs formed a regulatory network to simultaneously regulate miR-3065-3p targeting Myo18a. The present study helps to comprehensively understand the molecular mechanisms and regulatory interaction networks during early inflammatory response.

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Section: Construction Of Co-expression Networkmentioning

confidence: 87%

Integrative analyses reveal RNA regulatory network in Ti particles induced inflammation

Jiang

Zhang

et al. 2021

Eur J Inflamm

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“…Also, the impact of miR-433 on the proliferative and mineralization abilities as well as cell death of dental pulp cells has been reported, which was proposed to contribute to dental pulp repair and regeneration [28]. In dental papillary cells, Li et al observed that miR-3065-5p promoted odontoblastic differentiation through directly targeting Bmpr2 in late odontoblast differentiation [29].…”

Section: Discussionmentioning

confidence: 99%

The suppressive effects of miR-508-5p on the odontogenic differentiation of human dental pulp stem cells by targeting glycoprotein non-metastatic melanomal protein B

et al. 2019

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BackgroundAlthough the involvement of glycoprotein non-metastatic melanomal protein B (GPNMB) in regulating the odontogenic differentiation of human dental pulp stem cells (hDPCs) has been identified, the underlying mechanisms are largely unknown. The purpose of this study is to investigate the effects of miR-508-5p on the GPNMB expression and the odontogenic differentiation of hDPCs.MethodsIn this study, hDPCs were isolated and identified by flow cytometric analysis. Based on bioinformatics analysis, dual luciferase reporter assay was performed to verify GPNMB acting as a target of miR-508-5p. The regulatory roles of miR-508-5p in odontogenetic differentiation of hDPCs were investigated through its inhibition or overexpression (miRNA mimics and miRNA inhibitors). qRT-PCR and Western blot analysis were used to detect the expression of odontogenetic marker genes and proteins. The assays of alkaline phosphatase (ALP) activity and Alizarin Red S staining were performed to evaluate the odontogenetic phenotype.ResultsWe first found that the levels of miR-508-5p expression decreased gradually during odontogenesis of hDPCs, while the expressions of GPNMB were upregulated obviously. The suppressive effects of miR-508-5p on GPNMB were determined by oligonucleotide transfection in hDPCs and dual luciferase reporter assay in 293T cells. Subsequently, the significant inhibition of hDPC odontogenesis after the overexpression of miR-508-5p was observed, which is consistent with the decreased expression levels of several odontoblast-specific genes, such as dentin matrix protein 1 (DMP-1), dentin sialophosphoprotein (DSPP), and osteocalcin (OCN), as well as the decreased activity of ALP and weakened Alizarin Red S staining. Furthermore, ectopic expression of GPNMB (lacking 3′-UTR) rescued the effects of miR-508-5p on odontogenic differentiation.ConclusionsOur study demonstrated that miR-508-5p regulated the osteogenesis of hDPCs by targeting GPNMB and provided novel insight into the critical roles of microRNAs in hDPC differentiation.

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“…Odontoblastic differentiation of DPSCs involves many factors such as biological scaffolds, regulatory genes and signal pathways [4,14,22,26,27]. MicroRNAs (miRNAs, miRs) as posttranscriptional inhibitors, recognize and bind to the 3'untranslated region (3'UTR) of the target gene to inhibit the translation of the target gene protein, and have complex regulatory effects on the body's physiological/pathological activities, including the process of odontoblastic differentiation [10][11][12]. Long non-coding RNAs (LncRNAs) as competing endogenous RNAs (ceRNAs) play key role in cell cycle, migration, proliferation, differentiation and apoptosis through sponging miRNAs to regulate miRNA targets.…”

Section: Introductionmentioning

confidence: 99%

LncRNA-KCNQ1OT1 Promotes the Odontoblastic Differentiation of Dental Pulp Stem Cells via Regulating miR-153-3p/RUNX2 Axis

Lü

Zhang

et al. 2022

Preprint

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Background and Objective: Long non-coding RNAs (LncRNAs) play a key role in the odontoblastic differentiation. This study aimed to explore the role of LncRNA-KCNQ1OT1 in the odontoblastic differentiation of human dental pulp stem cells (DPSCs) and its possible mechanism. Methods: The expression of LncRNA-KCNQ1OT1, miR-153-3p, RUNX2 in the odontoblastic differentiation was detected by qRT-PCR. Interaction between LncRNA-KCNQ1OT1 and miR-153-3p and interaction between miR-153-3p and RUNX2 were detected by dual-luciferase assay. The cell viability of DPSCs was detected by cell counting kit-8 (CCK-8), and the effect of LncRNA-KCNQ1OT1 and miR-153-3p on the odontoblastic differentiation of DPSCs was observed by alizarin red staining, alkaline phosphatase (ALP) activity assay and Western blot for RUNX2, DSPP, DMP-1. Results: During odontoblastic differentiation of DPSCs, the expression of LncRNA-KCNQ1OT1 increased, miR-153-3p expression decreased, and RUNX2 expression increased. Dual-luciferase assay showed that LncRNA-KCNQ1OT1 sponges miR-153-3p and miR-153-3p targets on RUNX2. After LncRNA-KCNQ1OT1 and miR-153-3p expressions of DPSCs were changed, the cell viability was not notably changed, but the odontoblastic differentiation was notably changed which was confirmed with alizarin red staining, ALP activity and Western blot for RUNX2, DSPP, DMP-1. Conclusion: LncRNA-KCNQ1OT1 promotes the odontoblastic differentiation of DPSCs via regulating miR-153-3p/RUNX2 axis, which may provide a therapeutic clue for odontogenesis.

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miR-3065-5p regulates mouse odontoblastic differentiation partially through bone morphogenetic protein receptor type II

Cited by 9 publications

References 22 publications

Integrative analyses reveal RNA regulatory network in Ti particles induced inflammation

Integrative analyses reveal RNA regulatory network in Ti particles induced inflammation

The suppressive effects of miR-508-5p on the odontogenic differentiation of human dental pulp stem cells by targeting glycoprotein non-metastatic melanomal protein B

LncRNA-KCNQ1OT1 Promotes the Odontoblastic Differentiation of Dental Pulp Stem Cells via Regulating miR-153-3p/RUNX2 Axis

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