Abstract
PURPOSE: To study the effect of fluoride on autophagy in rat ameloblasts both in vitro and in vivo.
METHODS: Logarithmic-phase HAT-7 cells were cultured in different concentrations of fluoride for 48h. Transmission electron microscopy (TEM) was used to detect autophagosomes. Western blot and RT-qPCR were carried out to examine the expression of LC3 and Beclin 1. Forty Wistar rats were divided into 4 groups randomly. The expression of LC3 and Beclin 1 in rats was investigated by immunohistochemical staining in vivo. The data were analysed using SPSS13.0 software package.
RESULTS: The amount of autophagosomes in the experimental group was significantly more than that in the control group (P<0.05). The expression of LC3 and Beclin 1 were up-regulated in dose dependent manner after treatment with fluoride. Regression analysis showed that fluoride dependently induced the expression of LC3 and Beclin 1 (P<0.05).Immunohistochemical analysis revealed that the expression of LC3 and Beclin 1 in rat ameloblasts in the experimental groups was positive compared to control group.
CONCLUSIONS: Excessive fluoride induced autophagy in ameloblasts both in vitro and in vivo.
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Excessive fluoride induces endoplasmic reticulum stress and interferes enamel proteinases secretion
Protein retention in the enamel layer during tooth formation is well known to be associated with dental fluorosis but the underlying mechanism is unclear. The functions of the endoplasmic reticulum (ER) correlate directly with secreted protein metabolism. We used an ameloblast-derived cell line to determine whether excessive amounts of fluoride
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Fluoride affects enamel protein content via TGF-B1-mediated KLK4 inhibition
Dental fluorosis is caused by chronic high-level fluoride (F-) exposure during enamel development, and fluorosed enamel has a higher than normal protein content. Matrix metalloproteinase 20 cleaves enamel matrix proteins during the secretory stage, and KLK4 further cleaves these proteins during the maturation stage so that the proteins can be
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Fluoride Alters Klk4 Expression in Maturation Ameloblasts through Androgen and Progesterone Receptor Signaling.
Fluorosed maturation stage enamel is hypomineralized in part due to a delay in the removal of matrix proteins to inhibit final crystal growth. The delay in protein removal is likely related to reduced expression of kallikrein-related peptidase 4 (KLK4), resulting in a reduced matrix proteinase activity that found in fluorosed
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Dental fluorosis: variability among different inbred mouse strains.
Concurrent with the decline in dental caries has been an increase in the prevalence of dental fluorosis, a side-effect of exposure to greater than optimal levels of fluoride during amelogenesis. The mechanisms that underlie the pathogenesis of dental fluorosis are not known. We hypothesize that genetic determinants influence an individual's
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Developmental and post-eruptive defects in molar enamel of free-ranging Eastern Grey kangaroos (Macropus giganteus) exposed to high environmental levels of fluoride
Dental fluorosis has recently been diagnosed in wild marsupials inhabiting a high-fluoride area in Victoria, Australia. Information on the histopathology of fluorotic marsupial enamel has thus far not been available. This study analyzed the developmental and post-eruptive defects in fluorotic molar enamel of eastern grey kangaroos (Macropus giganteus) from the
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