To investigate the effect of different concentrations of fluoride on the expression of endoplasmic reticulum chaperone, and to explore the mechanism of dental fluorosis in rat.
Thirty Wistar rats were randomly divided into 3 groups. Immunohistochemistry was used to detect the expression of CRT, GRP78, XBP-1 and caspase-12 in rat incisors. Metamorph microscope images analysis system and SPSS 13.0 software package was used to analyze the data.
Typical features of dental fluorosis were found in the fluoride group. Results of immunohistochemistry showed that CRT (F=238.6, P<0.05), GRP78 (F=27.42, P<0.05), XBP-1 (F=139.7, P<0.05) and caspase-12 (F=43.91, P<0.05) were significantly different among the 3 groups.
Excessive fluoride can increase the secretion of CRT, GRP78, XBP-1 and caspase-12 suggest the ameloblasts and in status of endoplasmic reticulum stress and caspase-12 plays an important role during ameloblast apoptosis. Supported by National Natural Science Foundation of China (81072245) and Natural Science Foundation of Liaoning Province (20102278).
Fluoride induced endoplasmic reticulum stress and calcium overload in ameloblasts
OBJECTIVE: The aim of the study was to evaluate the involvement of endoplasmic reticulum stress and intracellular calcium overload on the development of dental fluorosis. METHODS: We cultured and exposed rat ameloblast HAT-7 cells to various concentrations of fluoride and measured apoptosis with flow cytometry and intracellular Ca2+ changes using confocal
Sirtuin1 and autophagy protect cells from fluoride-induced cell stress
Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase functioning in the regulation of metabolism, cell survival and organismal lifespan. Active SIRT1 regulates autophagy during cell stress, including calorie restriction, endoplasmic reticulum (ER) stress and oxidative stress. Previously, we reported that fluoride induces ER-stress in ameloblasts responsible for enamel formation,
Effect of siRNA PERK on fluoride-induced osteoblastic differentiation in OS732 cells
The purpose of this work is to study the action of fluoride on osteoblastic function through knocking down double-stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK) mRNA in OS732 cells (human osteoblast-like cell line). The previous researches had demonstrated that fluoride induced endoplasmic reticulum (ER) stresses in other cells or
LS8 cell apoptosis induced by NaF through p-ERK and p-JNK - a mechanism study of dental fluorosis
OBJECTIVE: To investigate the possible biological mechanism of dental fluorosis at a molecular level. MATERIAL AND METHODS: Cultured LS8 were incubated with serum-free medium containing selected concentrations of NaF (0???2?mM) for either 24 or 48?h. Subcellular microanatomy was characterized using TEM; meanwhile, selected biomolecules were analysed using various biochemistry techniques. Transient
Excessive ER stress and the resulting autophagic flux dysfunction contribute to fluoride-induced neurotoxicity.
Highlights Excessive ER stress plays an important role in NaF-induced neurotoxicity. NaF-induced neuronal death is caused by ER stress-elicited apoptosis and the impaired autophagic flux. Impaired autophagic flux was mediated by excessive ER stress in NaF-induced neurotoxicity. Fluoride is capable of inducing neurotoxicity, but its mechanisms remain elusive. This study
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