Sodium fluoride-induced autophagy of ameloblast-like cells via the p-ULk1/ATG13/LC3B pathway in vitro.

IF 2.9 3区医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Oral diseases Pub Date : 2024-10-01 Epub Date: 2024-02-06 DOI:10.1111/odi.14884

S Yang, D Song, R Wang, M Liu, T Tan, Y Wang, Q Xie, L Wang

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引用次数: 0

Abstract

Objective: To investigate the effects of sodium fluoride on the ameloblast and reveal the mechanism of dental fluorosis.

Materials and methods: Mouse ameloblast-like cell line (ALC) cells were treated with various concentrations of NaF, and subjected to Incucyte, fluorescence immunoassay, transmission electron microscopy, reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blot for autophagy examination, alkaline phosphatase and alizarin red staining for mineralization after osteogenic induction.

Results: NaF exerts a dose-dependent inhibitory effect on ALC cell growth. TEM and fluorescence immunoassay showed that 1.5 mM or higher concentrations of NaF could induce a fusion of lysosome and mitochondria, finally increasing the number of autophagosome. RT-qPCR and western blot showed that the upregulation of autophagy related gene 13 (ATG13), downregulation of phosphorylated Unc-51-like kinase 1 (p-ULK1) were found in NaF-induced autophagy of ALC cells. The knockdown of ATG13 could rescue it as well as the expression of p-ULK1 and LC3B. Besides, alizarin red staining showed that fluoride under these concentrations could promote the mineralization of ALC.

Conclusions: The data show that fluoride in higher concentration can induce autophagy via the p-ULk1/ATG13/LC3B pathway of ALCs than lower ones promote mineralization in vitro, which provides insight into the function of NaF in the autophagy and mineralization of ameloblast.

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氟化钠通过p-ULk1/ATG13/LC3B途径诱导体外羊膜样细胞自噬

目的研究氟化钠对牙釉质细胞的影响，揭示氟斑牙的发生机制：用不同浓度的NaF处理小鼠成髓细胞样细胞系（ALC），并对其进行Incucyte、荧光免疫分析、透射电子显微镜、逆转录定量聚合酶链反应（RT-qPCR）、自噬检测的Western blot、碱性磷酸酶和成骨诱导后矿化的茜素红染色：结果：NaF对ALC细胞的生长具有剂量依赖性抑制作用。TEM和荧光免疫分析表明，1.5 mM或更高浓度的NaF可诱导溶酶体和线粒体融合，最终增加自噬体的数量。RT-qPCR和Western印迹显示，在NaF诱导的ALC细胞自噬过程中，自噬相关基因13（ATG13）上调，磷酸化Unc-51样激酶1（p-ULK1）下调。敲除ATG13可以挽救自噬以及p-ULK1和LC3B的表达。此外，茜素红染色显示，这些浓度的氟化物可促进ALC的矿化：数据显示，高浓度的氟化物能通过p-ULk1/ATG13/LC3B途径诱导ALC自噬，而低浓度的氟化物则能促进体外ALC矿化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Oral diseases 医学-牙科与口腔外科

CiteScore

7.60

自引率

5.30%

发文量

325

审稿时长

4-8 weeks

期刊介绍： Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.