自噬
液泡
自噬体
氟化物
成釉细胞
PI3K/AKT/mTOR通路
氟化钠
化学
细胞内
细胞生物学
细胞器
氟斑牙
免疫组织化学
男科
生物
内科学
牙科
细胞凋亡
生物化学
医学
细胞质
搪瓷漆
无机化学
作者
Shuang Lei,Ying Zhang,Zhang Kaiqiang,Li J,Lu Liu
出处
期刊:Cells Tissues Organs
[S. Karger AG]
日期:2014-01-01
卷期号:200 (6): 405-412
被引量:17
摘要
Exposure to high levels of fluoride (F-) can result in dental fluorosis in different individuals, but the mechanism of dental fluorosis remains unclear. Autophagy is a highly conserved intracellular digestion process that degrades damaged organelles and protein aggregates. This study examined the effect of sodium fluoride (NaF) on the expression of Beclin1 and mTOR to elucidate the development mechanisms of dental fluorosis. HAT-7 cells were incubated with various concentrations of NaF, and autophagic vacuoles were studied by transmission electron microscopy. At both mRNA and protein level, expression of Beclin1, which is required for autophagosome formation and decreases the expression of mTOR, an autophagy-related complex, was increased at 1.2 mmol/l NaF compared to baseline (0 mmol/l NaF). Additionally, immunohistochemical analysis was performed on paraffin-embedded rat incisor sections to identify the expression of Beclin1 and mTOR proteins in vitro. Highly significant differences were detected compared to controls. In summary, our results demonstrate unequivocally that excessive amounts of fluoride cause autophagy of HAT-7 cells, indicating that autophagy is involved in dental fluorosis.
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