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氟化物暴露会改变釉质细胞中的钙信号和线粒体功能。

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

机构信息

Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY 10010, USA.

Biology Program, Division of Science and Mathematics, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates.

出版信息

Sci Signal. 2020 Feb 18;13(619):eaay0086. doi: 10.1126/scisignal.aay0086.

DOI:10.1126/scisignal.aay0086
PMID:32071168
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7173621/
Abstract

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 signaling. Primary enamel cells and an enamel cell line (LS8) exposed to fluoride showed decreased internal Ca stores and store-operated Ca 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 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 channel IPR and the activity of the sarco-endoplasmic reticulum Ca-ATPase (SERCA) pump during Ca 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.

摘要

氟离子具有高度的反应性，其在低浓度下参与形成牙釉质，促进矿化。相比之下，过量的氟摄入会导致氟斑牙，这是一种肉眼可见的牙釉质缺陷，会增加龋齿的风险。为了研究氟斑牙的分子基础，我们分析了氟暴露对釉质细胞中钙信号的影响。暴露于氟化物的原代釉质细胞和釉质细胞系（LS8）显示出内部钙储存减少和钙库操纵性钙内流（SOCE）减少。RNA 测序分析显示，氟化物处理的 LS8 细胞中基因表达发生变化，提示内质网（ER）应激。氟化物暴露不会改变 Ca 稳态或增加 HEK-293 细胞中 ER 应激相关基因的表达。在釉质细胞中，氟化物暴露影响内质网局部钙通道 IPR 的功能和内质网钙填充过程中肌浆网-内质网 Ca-ATP 酶（SERCA）泵的活性。氟化物会对线粒体呼吸产生负面影响，引起线粒体膜去极化，并破坏线粒体形态。总之，这些数据为氟斑牙提供了一种潜在的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/962681a0a266/nihms-1574395-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/ea27476ad22d/nihms-1574395-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/3791454d0650/nihms-1574395-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/bf7547ffa69e/nihms-1574395-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/29006360a588/nihms-1574395-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/ab7c76dd4190/nihms-1574395-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/962681a0a266/nihms-1574395-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/ea27476ad22d/nihms-1574395-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/3791454d0650/nihms-1574395-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/bf7547ffa69e/nihms-1574395-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/29006360a588/nihms-1574395-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/ab7c76dd4190/nihms-1574395-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e2c/7173621/962681a0a266/nihms-1574395-f0006.jpg

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