ArticlePeerJ2019
Comprehensive analysis of an lncRNA-miRNA-mRNA competing endogenous RNA network in pulpitis.
Article in PeerJ, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- MicroRNA expression in apical periodontitis and pulpal inflammation: a systematic review.PeerJ · 2023Pooled it
- Dysregulation of miR-140-3p is involved in the pathogenesis of pulpitis via the regulation of ACSL1.Odontology · 2026Article
- Noncoding RNA networks in endodontic regeneration: Current evidence and future directions.Journal of conservative dentistry and endodontics · 2026Review
- Long non-coding RNA FOXD2-AS1 promotes inflammation but suppresses osteogenesis in pulpitis via miR-338-3p/THBS1 axis.Odontology · 2026Article
- Dysregulation of Pulpitis Progression Through Modulation of the lncRNA ITGB2-AS1 /miR-1224-5p Axis.International dental journal · 2026Article
- A novel NUTM2A-AS1/miR-769-5p axis regulates LPS-evoked damage in human dental pulp cells via the TLR4/MYD88/NF-κB signaling.Journal of dental sciences · 2025Article
- Identification of pain-related long non-coding RNAs for pulpitis prediction.Clinical oral investigations · 2025Article
- Current Insights into the Roles of LncRNAs and CircRNAs in Pulpitis: A Narrative Review.International journal of molecular sciences · 2024Review
- Developing a ceRNA-based lncRNA-miRNA-mRNA regulatory network to uncover roles in skeletal muscle development.Frontiers in bioinformatics · 2024Article
- DUXAP8 Promotes LPS-Induced Cell Injury in Pulpitis by Regulating miR-18b-5p/HIF3A.International dental journal · 2023Article
- Dysregulation of MicroRNA-152-3p is Associated with the Pathogenesis of Pulpitis by Modulating SMAD5.Oral health & preventive dentistry · 2023Article
- Establishment and validation of the autophagy-related ceRNA network in irreversible pulpitis.BMC genomics · 2023Article
- Identification of the characteristics of infiltrating immune cells in pulpitis and its potential molecular regulation mechanism by bioinformatics method.BMC oral health · 2023Article
- Identification and Experimental Validation of LINC00582 Associated with B Cell Immune and Development of Pulpitis: Bioinformatics and In Vitro Analysis.Diagnostics (Basel, Switzerland) · 2023Article
- Regulation mechanism and pathogenic role of lncRNA plasmacytoma variant translocation 1 (Genes & diseases · 2023Review
- Wnt4 prevents apoptosis and inflammation of dental pulp cells induced by LPS by inhibiting the IKK/NF‑κB pathway.Experimental and therapeutic medicine · 2023Article
- Identification and characterization of the ferroptosis-related ceRNA network in irreversible pulpitis.Frontiers in immunology · 2023Article
- Long Non-coding RNA PVT1 is Involved in the Pathological Mechanism of Pulpitis by Regulating miR-128-3p.Oral health & preventive dentistry · 2022Article
- Analysis of circRNAs profile in TNF-α treated DPSC.BMC oral health · 2022Article
- LncRNA OGFRP1 promotes cell proliferation and suppresses cell radiosensitivity in gastric cancer by targeting the miR-149-5p/MAP3K3 axis.Journal of molecular histology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulpitis is a common inflammatory disease that affects dental pulp. It is important to understand the molecular signals of inflammation and repair associated with this process. Increasing evidence has revealed that long noncoding RNAs (lncRNAs), via competitively sponging microRNAs (miRNAs), can act as competing endogenous RNAs (ceRNAs) to regulate inflammation and reparative responses. The aim of this study was to elucidate the potential roles of lncRNA, miRNA and messenger RNA (mRNA) ceRNA networks in pulpitis tissues compared to normal control tissues.
methodsThe oligo and limma packages were used to identify differentially expressed lncRNAs and mRNAs (DElncRNAs and DEmRNAs, respectively) based on expression profiles in two datasets, GSE92681 and GSE77459, from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were further analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Protein-protein interaction (PPI) networks and modules were established to screen hub genes using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and the Molecular Complex Detection (MCODE) plugin for Cytoscape, respectively. Furthermore, an lncRNA-miRNA-mRNA-hub genes regulatory network was constructed to investigate mechanisms related to the progression and prognosis of pulpitis. Then, quantitative real-time polymerase chain reaction (qRT-PCR) was applied to verify critical lncRNAs that may significantly affect the pathogenesis in inflamed and normal human dental pulp.
resultsA total of 644 upregulated and 264 downregulated differentially expressed genes (DEGs) in pulpitis samples were identified from the GSE77459 dataset, while 8 up- and 19 downregulated probes associated with lncRNA were identified from the GSE92681 dataset. Protein-protein interaction (PPI) based on STRING analysis revealed a network of DEGs containing 4,929 edges and 623 nodes. Upon combined analysis of the constructed PPI network and the MCODE results, 10 hub genes, including IL6, IL8, PTPRC, IL1B, TLR2, ITGAM, CCL2, PIK3CG, ICAM1, and PIK3CD, were detected in the network. Next, a ceRNA regulatory relationship consisting of one lncRNA (PVT1), one miRNA (hsa-miR-455-5p) and two mRNAs (SOCS3 and PLXNC1) was established. Then, we constructed the network in which the regulatory relationship between ceRNA and hub genes was summarized. Finally, our qRT-PCR results confirmed significantly higher levels of PVT1 transcript in inflamed pulp than in normal pulp tissues (
conclusionOur study identified a novel lncRNA-mediated ceRNA regulatory mechanisms in the pathogenesis of pulpitis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.