ArticleJournal of cellular and molecular medicine2018
METTL3 regulates alternative splicing of MyD88 upon the lipopolysaccharide-induced inflammatory response in human dental pulp cells.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.
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Who cites it
127 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis-A Systematic Review.Biomolecules · 2022Pooled it
- Regulation of RNA-binding proteins by small biomolecules.Nature reviews. Molecular cell biology · 2026Review
- Article
- IGF2BP3/m6A-mediated intron retention isoform of DUSP6 promotes cisplatin resistance in nasopharyngeal carcinoma by inhibiting pyroptosis.BMC cancer · 2026Article
- METTL3 and METTL14 drive pancreatic adenocarcinoma progression via m6A-dependent alternative splicing in PANC-1 cells.Discover oncology · 2025Article
- Rethinking RNA Modifications: Therapeutic Strategies for Targeting Dysregulated RNA.Journal of molecular biology · 2025Review
- N6-Methyladenosine Modification in the Metabolic Dysfunction-Associated Steatotic Liver Disease.Nutrients · 2025Review
- LincRNA-ASAO promotes dental pulp repair through interacting with PTBP1 to increase ALPL alternative splicing.Stem cell research & therapy · 2025Article
- The potential impact of RNA splicing abnormalities on immune regulation in endometrial cancer.Cell death & disease · 2025Review
- Alternative Splicing of Pre-mRNA Matters in Oral Diseases.Current gene therapy · 2025Review
- Epigenetic orchestration of RNA mInternational journal of biological sciences · 2025Review
- Intestinal Epithelial Cell-specific Knockout of METTL3 Aggravates Intestinal Inflammation in CLP Mice by Weakening the Intestinal Barrier.Current pharmaceutical biotechnology · 2025Article
- Toll-like receptors and their role in the pathogenesis of myasthenia gravis: a comprehensive review.Frontiers in immunology · 2025Review
- Application of methylation in the diagnosis of ankylosing spondylitis.Clinical rheumatology · 2024Review
- RNA m6A methylation regulators in sepsis.Molecular and cellular biochemistry · 2024Review
- Inhibition of METTL3 Alleviates NLRP3 Inflammasome Activation via Increasing Ubiquitination of NEK7.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Single-molecule epitranscriptomic analysis of full-length HIV-1 RNAs reveals functional roles of site-specific mNature microbiology · 2024Article
- mViruses · 2024Review
- Dysregulated NFrontiers of medicine · 2024Article
- Review
67 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dental pulp inflammation is a widespread public health problem caused by oral bacterial infections and can progress to pulp necrosis and periapical diseases. N6-methyladenosine (m6A) is a prevalent epitranscriptomic modification in mRNA. Previous studies have demonstrated that m6A methylation plays important roles in cell differentiation, embryonic development and stress responses. However, whether m6A modification affects dental pulp inflammation remains unknown. To address this issue, we investigated the expression of m6A and N6-adenosine methyltransferase (METTL3, METTL14) as well as demethylases (FTO, ALKBH5) and found that the levels of m6A and METTL3 were up-regulated in human dental pulp cells (HDPCs) stimulated by lipopolysaccharide (LPS). Furthermore, we knocked down METTL3 and demonstrated that METTL3 depletion decreased the expression of inflammatory cytokines and the phosphorylation of IKKα/β, p65 and IκBα in the NF-κB signalling pathway as well as p38, ERK and JNK in the MAPK signalling pathway in LPS-induced HDPCs. The RNA sequencing analysis revealed that the vast number of genes affected by METTL3 depletion was associated with the inflammatory response. Previous research has shown that METTL3-dependent N6-adenosine methylation plays an important role in mRNA splicing. In this study, we found that METTL3 knockdown facilitated the expression of MyD88S, a splice variant of MyD88 that inhibits inflammatory cytokine production, suggesting that METTL3 might inhibit the LPS-induced inflammatory response of HDPCs by regulating alternative splicing of MyD88. These data shed light on new findings in epitranscriptomic regulation of the inflammatory response and open new avenues for research into the molecular mechanisms of dental pulp inflammation.
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