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ABSTRACT:
PROVIDER: PRJNA1283556 | ENA |
REPOSITORIES: ENA
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Project description:Although an appropriate range of fluoride is thought to be safe and effective, excessive fluoride intake results in toxic effects in either hard tissues of teeth and skeleton or soft tissues of kidney, lung and brain. It is also well known that fluoride at a millimolar range elicits the complex cellular responses such as enzyme activity, signal transduction and apoptosis in many kinds of cells. However, its toxic effects are still unclear. In this study, to identify genes involved in cell death induced by sodium fluoride (NaF) in rat oral epithelial ROE2 cells, global-scale gene expression analysis was carried out using a GeneChip® system.
2014-01-09 | GSE53937 | GEO
Project description:Although an appropriate range of fluoride is thought to be safe and effective, excessive fluoride intake results in toxic effects in either hard tissues of teeth and skeleton or soft tissues of kidney, lung and brain. It is also well known that fluoride at a millimolar range elicits the complex cellular responses such as enzyme activity, signal transduction and apoptosis in many kinds of cells. However, its toxic effects are still unclear. In this study, to identify genes involved in apoptosis induced by sodium fluoride (NaF) in rat oral epithelial ROE2 cells, global-scale gene expression analysis was carried out using a GeneChipM-BM-. system. NaF (2 mM) significantly induced apoptosis accompaning chromatin condensation and caspase-3 activation. Total RNA samples were prepared from the NaF-treated cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was monitored by an Affymetrix GeneChipM-BM-. system with a Rat Genome 230 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerM-bM-^@M-^Ys instructions.
2014-01-09 | E-GEOD-53937 | biostudies-arrayexpress
Project description: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 Bax, p21, and Mdm2 genes and upregulated their mRNA levels. Fluoride decreased H3K27ac peaks and p53, Bad, and Bcl2 had suppressed transcription. HAT inhibitors (Anacardic acid or MG149) suppressed fluoride-induced mRNA of p21 and Mdm2, while fluoride and the histone deacetylase (HDAC) inhibitor sodium butyrate increased Bad and Bcl2 expression above that of fluoride treatment alone. To our knowledge, this is the first study that demonstrates epigenetic regulation via fluoride treatment via H3 acetylation. Further investigation is required to elucidate epigenetic mechanisms of fluoride toxicity in enamel development.
2026-07-14 | GSE337787 | GEO
Project description:Identification of genes involved in cell death induced by sodium fluoride in rat oral epithelial cells
| PRJNA233998 | ENA
Project description:EFFECTS OF SODIUM FLUORIDE OVER ORAL BACTERIAL BIOFILMS COMPOSITION AND ACTIVITY
| PRJEB35662 | ENA
Project description:RNA-Seq of FEX1, FEX2 deleted S. cerevisiae (yeast) treated with sodium fluoride against untreated control
| PRJEB33061 | ENA
Project description:Though fluoride is considered an essential trace element, chronic exposure to fluoride is known to cause toxic effects. Chronic exposure of high concentration of fluoride may leads to fluorosis. To understand the molecular mechanism of fluoride induced toxicity gene expression profiling was performed on osteosarcoma cells (HOS). Cells were exposed to sub-lethal concentration of fluoride (8 ppm) for 30 days. Our result demonstrates that fluoride alters multiple biological pathways including bone development, osteoblast differentiation and apoptotic pathways. HOS cells grown in MEM were treated with fluoride and total RNA was isolated from cells after 30 days exposure. Three replicates per group were used for the experiment.
2016-06-30 | E-GEOD-70719 | biostudies-arrayexpress
Project description:To understand the function of MFG-e8, which is secreted from human embryonic stem cells (hESCs), hESC line BG01 cells were treated with anti-M8nAb to deplete the MFG-e8 activity. Depletion of MFG-e8 activity in hESC cultures resulted in decreased cell proliferation, increased cell death, and prominent morphological changes within 2 days. To investigate the transcriptomic changes under depletion of MFG-e8 activity in hESC culture, we performed RNA-seq analysis of BG01 cells treated with anti-M8nAb at two different time point. As a result, we identified differentially expressed genes in anti-M8nAb treated BG01 cells compared to isotype IgG treated control cells. Transcriptome of anti-M8nAb tretaed BG01 cells were enriched with the genesets related with cell death, cell cycle arrest, and epithelial-to-mesenchymal transition compared to isotype IgG treated control cells. In conclusion, these RNA-seq analysis results can provide insights into how MFG-e8 affect signaling mechanisms in hESCs.
2025-04-02 | GSE276921 | GEO
Project description:Fluoride toxicity in multiple organs has been extensively reported in several decades of research. In-depth study coverage is available on teeth and bone tissues. But studies addressing skeletal muscle fluorosis are scanty. C57BL/6 mice were provided with sodium fluoride in drinking water for 60 days. Histological analysis, primary culture of skeletal muscle was performed. Protein expressions were analyzed by Immunocytochemistry, qRT-PCR, and western blotting techniques. Proteomic approach was considered to overview the entire proteome response. Exposure to sodium fluoride resulted in the loss of body weight in C57BL/6 mice. The compactness of the myofibre arrangement was distorted due to the treatment. Major reduction of contractile proteins such as actinin, troponin, and myosin further loss of mitochondrial proteins were confirmed by proteomic approach. Sodium fluoride treatment altered mitochondrial function. Further, loss of contractile proteins triggered skeletal muscle weakness.
2023-03-11 | PXD035014 | Pride