Fluoride exposure alters Ca 2+ signaling and mitochondrial function in enamel cells.

Autor: Aulestia FJ; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY 10010, USA., Groeling J; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY 10010, USA., Bomfim GHS; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY 10010, USA., Costiniti V; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY 10010, USA., Manikandan V; Biology Program, Division of Science and Mathematics, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates., Chaloemtoem A; Biology Program, Division of Science and Mathematics, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates., Concepcion AR; Department of Pathology, New York University School of Medicine, New York, NY 10016, USA., Li Y; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY 10010, USA., Wagner LE 2nd; Department of Pharmacology and Physiology, University of Rochester, Rochester, NY 14526, USA., Idaghdour Y; Biology Program, Division of Science and Mathematics, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates., Yule DI; Department of Pharmacology and Physiology, University of Rochester, Rochester, NY 14526, USA., Lacruz RS; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY 10010, USA. rodrigo.lacruz@nyu.edu.
Jazyk: angličtina
Zdroj: Science signaling [Sci Signal] 2020 Feb 18; Vol. 13 (619). Date of Electronic Publication: 2020 Feb 18.
DOI: 10.1126/scisignal.aay0086
Abstrakt: 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 Ca 2+ signaling. Primary enamel cells and an enamel cell line (LS8) exposed to fluoride showed decreased internal Ca 2+ stores and store-operated Ca 2+ 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 Ca 2+ 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 Ca 2+ channel IP 3 R and the activity of the sarco-endoplasmic reticulum Ca 2+ -ATPase (SERCA) pump during Ca 2+ 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.
(Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
Databáze: MEDLINE
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