ArticleInternational journal of molecular sciences2024
Fluoride Alters Gene Expression via Histone H3K27 Acetylation in Ameloblast-like LS8 Cells.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Quantification of Fluoride in Serum, Bone, and Teeth in a Murine Model Using Hexamethyldisiloxane-Facilitated Diffusion and Ion-Selective Electrode Measurements.Journal of visualized experiments : JoVE · 2026Article
- Human Enamel Formation: A Scoping Review for Oral Health Professionals.Dentistry journal · 2026Review
- Effects of Fluoride and 8:2 FTOH on β-Cell Calcium Signaling and Insulin Homeostasis: An Exploratory Study.Metabolites · 2026Article
- Developmental vulnerability to fluoride toxicity: enamel and clearance differences in adolescent versus mature mice.Archives of toxicology · 2026Article
- Metabolic programming in tooth development: a regulatory network from energy substrates to signaling instructions.Frontiers in cell and developmental biology · 2026Review
- Salivary Proteomic Signatures Reveal Novel Mechanistic Insights into Moderate Dental Fluorosis Pathogenesis and Oral Homeostasis Disruption.Computational and structural biotechnology journal · 2026Article
- Differentiation of rat bone marrow mesenchymal stem cell into uterine smooth muscle cellOpen life sciences · 2026Article
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Authors and funding
15 authors.
Funding
Abstract
Excessive fluoride ingestion during tooth development can cause dental fluorosis. Previously, we reported that fluoride activates histone acetyltransferase (HAT) to acetylate p53, promoting fluoride toxicity in mouse ameloblast-like LS8 cells. However, the roles of HAT and histone acetylation status in fluoride-mediated gene expression remain unidentified. Here, we demonstrate that fluoride-mediated histone modification causes gene expression alterations in LS8 cells. LS8 cells were treated with or without fluoride followed by ChIP-Seq analysis of H3K27ac. Genes were identified by differential H3K27ac peaks within ±1 kb from transcription start sites. The levels of mRNA of identified genes were assessed using rea-time PCR (qPCR). Fluoride increased H3K27ac peaks associated with
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