ArticleJournal of dental sciences2023
Circ_0138960 knockdown alleviates lipopolysaccharide-induced inflammatory response and injury in human dental pulp cells by targeting miR-545-5p/MYD88 axis in pulpitis.
Article in Journal of dental sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Circ_0043582 promotes dental pulp cell injury via miR-940/TRAF3/NF-κB axis in pulpitis.Odontology · 2026Article
- Molecular mechanism by which mir-153-3p attenuates pulpitis in human deciduous teeth via PTEN-targeted suppression of inflammation and oxidative stress.Odontology · 2026Article
- Dysregulation of Pulpitis Progression Through Modulation of the lncRNA ITGB2-AS1 /miR-1224-5p Axis.International dental journal · 2026Article
- The circ_0042103/TAF15/NER axis regulates inflammation and DNA damage in pulpitis.Stem cell research & therapy · 2026Article
- Mechanistic insights into dental stem cells-derived exosomes in regenerative endodontics.International endodontic journal · 2025Review
- Potential of Dental Pulp Stem Cell Exosomes: Unveiling miRNA-Driven Regenerative Mechanisms.International dental journal · 2025Review
- Current Insights into the Roles of LncRNAs and CircRNAs in Pulpitis: A Narrative Review.International journal of molecular sciences · 2024Review
- A carbon dot nanozyme hydrogel enhances pulp regeneration activity by regulating oxidative stress in dental pulpitis.Journal of nanobiotechnology · 2024Article
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
Background/purpose: Circular RNAs (circRNAs) have been shown to play important regulatory roles in many human diseases, yet their functions in pulpitis remain to be clarified. This study was designed to investigate the function of circ_0138960 in pulpitis progression and its underlying mechanism. Material and methods: Cell viability and proliferation were analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and 5-Ethynyl-2'-deoxyuridine (EdU) assay. Flow cytometry and enzyme-linked immunosorbent assay (ELISA) were conducted to analyze cell apoptosis rate and the release of inflammatory cytokines. The activity of superoxide dismutase (SOD) was analyzed using a SOD assay kit. Dual-luciferase reporter and RNA-pull down assays were performed to verify the interaction between microRNA-545-5p (miR-545-5p) and circ_0138960 or myeloid differentiation primary response gene 88 (MYD88). Results: Lipopolysaccharide (LPS) treatment restrained the proliferation and promoted the apoptosis, inflammation, and oxidative stress of human dental pulp cells (hDPCs). LPS treatment dose-dependently up-regulated circ_0138960 expression in hDPCs. Circ_0138960 knockdown overturned LPS-induced inflammation and injury in hDPCs. Circ_0138960 could act as a molecular sponge for miR-545-5p, and circ_0138960 knockdown protected hDPCs from LPS-induced effects by up-regulating miR-545-5p. miR-545-5p directly interacted with the 3' untranslated region (3'UTR) of MYD88, and MYD88 overexpression reversed miR-545-5p-mediated effects in LPS-treated hDPCs. Circ_0138960 positively regulated MYD88 expression by sponging miR-545-5p in hDPCs. LPS could activate nuclear factor kappa-B (NF-κB) signaling by targeting circ_0138960/miR-545-5p/MYD88 axis in hDPCs. Conclusion: Circ_0138960 knockdown attenuated LPS-induced inflammatory response and injury in hDPCs by targeting the miR-545-5p/MYD88/NF-κB axis.
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Registered trials
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.