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).
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,
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
[Effects. of N-acetylcysteine on fluoride-induced endoplasmic reticulum stress in sertoli cells].
OBJECTIVE: Investigated the effects of N-acetylcysteine (NAC) on endoplasmic reticulum stress of sertoli cells induced by sodium fluoride (NaF). METHODS: Rat sertoli cells were exposed to various concentration of (0, 6, 12, 24 µg/ml) sodium fluoride with or without 2 mmol/L NAC for 24 hours. The cell viability was evaluated using
Sodium fluoride induces apoptosis through reactive oxygen species-mediated endoplasmic reticulum stress pathway in Sertoli cells
Excessive fluoride exposure is known to contribute to reproductive system dysfunction, ultimately leading to pathological damage and apoptosis in cells. Although both oxidative and endoplasmic reticulum (ER) stresses have been implicated in fluorosis, the signaling pathways and their roles in sodium fluoride (NaF)-induced apoptosis of Sertoli cells have been sparsely
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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