Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1003010 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25551239_1.fastq.gz | Fastqsanger.gz | |||
| SRR25551239_2.fastq.gz | Fastqsanger.gz | |||
| SRR25551240_1.fastq.gz | Fastqsanger.gz | |||
| SRR25551240_2.fastq.gz | Fastqsanger.gz | |||
| SRR25551241_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
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: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.
2016-06-30 | GSE70719 | GEO
Project description:Fluorosis is caused due to excess of fluoride intake over a long period of time. Aberrant change in RUNX2-mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Till date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling ofshort non-coding RNAs, in particular miRNAs and snoRNAs was carried out in NaF treated HOS cells to understand their possible role in the development of fluorosis. RT-PCR and insilico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of RUNX2 and RANKL genes. Compare to control, C/D box analysis revealed mark elevation in the number of UG dinucleotides and D-box sequences in NaF exposed HOS cells. Herein, we report miR-124 and miR-155 as the new possible players involved in the development of fluorosis. We also state that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure. HOS cells grown on MEM media were treated with sodium fluoride and total RNA was isolated from cells after one month of chronic exposure; Cells grown on six 25mm flask. two replicates of control and two different concentration of exposed samples; two replicate are served as control
2015-01-01 | E-GEOD-57550 | biostudies-arrayexpress
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
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:Fluorosis is caused due to excess of fluoride intake over a long period of time. Aberrant change in RUNX2-mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Till date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling ofshort non-coding RNAs, in particular miRNAs and snoRNAs was carried out in NaF treated HOS cells to understand their possible role in the development of fluorosis. RT-PCR and insilico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of RUNX2 and RANKL genes. Compare to control, C/D box analysis revealed mark elevation in the number of UG dinucleotides and D-box sequences in NaF exposed HOS cells. Herein, we report miR-124 and miR-155 as the new possible players involved in the development of fluorosis. We also state that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure.
2015-01-01 | GSE57550 | GEO
Project description:In order to define the underlying mechanism of fluoride resistance in mammals and provide a theoretical basis for fluorosis treatment, high-throughput sequencing was applied to map the genetic changes of fluoride-resistant mouse osteoblasts. Fluoride-tolerant MC3T3-E1 cells were developed by gradient fluoride exposure. The differentially expressed genes of fluorine-resistant MC3T3-E1 cells were identified by high-throughput sequencing. High-throughput RNA sequencing identified 2702 differentially expressed genes (DEGs) showed more than 2-fold difference in 30ppm FR MC3T3-E1 cells, of which 17 DEGs were associated with ferroptosis.
2022-05-25 | GSE203511 | 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 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:Exposure to excessive fluoride can lead to dental enamel hypomineralization characterized by retention of enamel matrix proteins(EMPs). However, the types and functions of EMPs from different fluoride exposure pathways remains elusive. This study selected moderate-to-severe coal-fired dental fluorosis enamel(CDF), water-drinking dental fluorosis enamel(WDF) and healthy permanent dental enamel (H) from the residents (local until age 12). EMPs were extracted, digested, and analyzed via nanoLC-HRMS/MS, followed by database searching and bioinformatics.
| PXD069233 |