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Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE143536 | GEO | 2020/01/14

REPOSITORIES: GEO

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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

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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

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]

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

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

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Hippocampal Subregions Express Distinct Dendritic Transcriptomes that Reveal Differences in Mitochondrial Function in CA2

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

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Inositol Trisphosphate Receptor Mediated Ca2+ Signalling Stimulates Mitochondrial Function and Gene Expression in Core Myopathy Patients

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Gata2 is a master regulator of endometrial function and progesterone signaling

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Mitochondrial Function in Enamel Development.

Project description:Enamel is the most calcified tissue in vertebrates. Enamel formation and mineralization is a two-step process that is mediated by ameloblast cells during their secretory and maturation stages. In these two stages, ameloblasts are characterized by different morphology and function, which is fundamental for proper mineral growth in the extracellular space. Ultrastructural studies have shown that the mitochondria in these cells localize to different subcellular regions in both stages. However, limited knowledge is available on the role/s of mitochondria in enamel formation. To address this issue, we analyzed mitochondrial biogenesis and respiration, as well as the redox status of rat primary enamel cells isolated from the secretory and maturation stages. We show that maturation stage cells have an increased expression of PGC1?, a marker of mitochondrial biogenesis, and of components of the electron transport chain. Oxygen consumption rate (OCR), a proxy for mitochondrial function, showed a significant increase in oxidative phosphorylation during the maturation stage, promoting ATP production. The GSH/GSSG ratio was lower in the maturation stage, indicative of increased oxidation. Because higher oxidative phosphorylation can lead to higher ROS production, we tested if ROS affected the expression of AmelX and Enam genes that are essential for enamel formation. The ameloblast cell line LS8 treated with H2O2 to promote ROS elicited significant expression changes in AmelX and Enam. Our data highlight important metabolic and physiological differences across the two enamel stages, with higher ATP levels in the maturation stage indicative of a higher energy demand. Besides these metabolic shifts, it is likely that the enhanced ETC function results in ROS-mediated transcriptional changes.

| S-EPMC7274036 | biostudies-literature

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