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Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells [Mouse]

ABSTRACT: Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells [Mouse]

PROVIDER: PRJNA600897 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10877167_1.fastq.gz	Fastqsanger.gz
	SRR10877167_2.fastq.gz	Fastqsanger.gz
	SRR10877168_1.fastq.gz	Fastqsanger.gz
	SRR10877168_2.fastq.gz	Fastqsanger.gz
	SRR10877169_1.fastq.gz	Fastqsanger.gz

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Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells [Mouse]

Project description:We analyzed the effects of fluoride exposure in mouse enamel cells to assess its impact on cell Ca2+ signaling

2020-01-14 | GSE143535 | GEO

Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells [Human]

Project description:We analyzed the effects of fluoride exposure in mouse enamel cells to assess its impact on cell Ca2+ signaling

2020-01-14 | GSE143534 | GEO

Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells

Project description:Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells

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Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells [Human]

Project description:Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells [Human]

| PRJNA600896 | ENA

Store operated Ca2+ entry (SOCE) controls ameloblast cell function and enamel development

Project description:Abstarct:Mutations in the endoplasmic reticulum (ER) Ca2+ sensor stromal interaction molecule 1 (STIM1) result is a number of disease states including abnormal enamel formation. However, these defects in enamel have remained unclear given a lack of animal models available. We generated Stim1/2K14Cre mice to ablate the activity of STIM1 and its homologue STIM2 in enamel cells. These mice showed impaired Ca2+ entry in enamel cells and although enamel formed, it was severely hypomineralized and mechanically weak. RNA-sequencing of enamel cells provided a global overview of loss of Ca2+ sensor activity. ER stress markers associated with unfolded protein response (UPR) were increased. Cell morphology was altered showing loss of the typical ruffled-border and mislocalized mitochondria. We also identified decreased glutathione system and potentially associated with this, increased ROS and abnormal mitochondria. The Ca2+ extrusion system and enamel gene expression were also altered. These data might represent the first in vivo study linking Stim1/2 ablation with increased UPR function, decreased glutathione metabolism, increased ROS and abnormal mitochondria. Loss of ER Ca2+ sensors Stim1/2 in enamel cells has substantial detrimental effects at the cell and mineral phase level.

2017-01-17 | GSE93655 | GEO

Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-01-14 | GSE143536 | GEO

Fluoride exposure alters Ca2+ signaling and mitochondrial function in enamel cells.

Project description:Fluoride ions are highly reactive, and their incorporation in forming dental enamel at low concentrations promotes mineralization. In contrast, excessive fluoride intake causes dental fluorosis, visually recognizable enamel defects that can increase the risk of caries. To investigate the molecular bases of dental fluorosis, we analyzed the effects of fluoride exposure in enamel cells to assess its impact on Ca2+ signaling. Primary enamel cells and an enamel cell line (LS8) exposed to fluoride showed decreased internal Ca2+ stores and store-operated Ca2+ entry (SOCE). RNA-sequencing analysis revealed changes in gene expression suggestive of endoplasmic reticulum (ER) stress in fluoride-treated LS8 cells. Fluoride exposure did not alter Ca2+ homeostasis or increase the expression of ER stress-associated genes in HEK-293 cells. In enamel cells, fluoride exposure affected the functioning of the ER-localized Ca2+ channel IP3R and the activity of the sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) pump during Ca2+ refilling of the ER. Fluoride negatively affected mitochondrial respiration, elicited mitochondrial membrane depolarization, and disrupted mitochondrial morphology. Together, these data provide a potential mechanism underlying dental fluorosis.

| S-EPMC7173621 | biostudies-literature

Gene expression profiling of HOS (human osteosarcoma) cells exposed to fluoride

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

Gene expression profiling of HOS (human osteosarcoma) cells exposed to fluoride

2016-06-30 | E-GEOD-70719 | biostudies-arrayexpress

Micromolar fluoride alters ameloblast lineage cells in vitro

Project description:Previously characterized ameloblast-lineage cells were used in this study to determine whether micromolar levels of fluoride could be directly affect these cells. Keywords: substance response

2007-07-20 | GSE5365 | GEO

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