Abstract

Highlights

• NaF exposure significantly decreased the proliferation rate of mouse osteoblast cells in a dose dependent manner.
• NaF exposure induced autophagy in the osteoblast cells with an increase in TGF-ß1 expression.
• Overexpression of TGF-ß1 enhanced NaF-induced autophagy.
• Silencing of TGF-ß1 reduced NaF-induced autophagy.

Abstract

It is well known that excess fluoride intake can result in fluorosis, which is a serious public health problem. TGF-ß1 affects a wide variety of cellular activities and plays an important role in fluorosis. Recent literature proved that fluoride induces autophagy, however, the mechanism is still unclear, and the role of TGF-ß1 in the fluoride-induced autophagy should be further illustrated. Therefore, in this study, plasmids and small interfering RNA (siRNA) were used to overexpress and silence the TGF-ß1 expression in the osteoblasts cells. Our results demonstrated that sodium fluoride (NaF) (2.26 mg/L F-) exposure lead to a significant decrease in proliferation rate of mouse osteoblast cells in a dose-dependent manner with a concomitant increase in the expression levels of TGF-ß1 and autophagic markers. Overexpression of TGF-ß1 significantly increased the fluorescence intensity of MDCstained cells, the mRNA and protein expression levels of Beclin1 and LC3-II/I, with a concomitant decrease in p62. However, TGF-ß1 silencing resulted in vice versa. In summary, we concluded that TGF-ß1 plays a mediator role in NaF-induced autophagy of mouse osteoblast cells. In the future, TGF-ß1-autophagy signaling network could be a new idea for the investigation of skeletal fluorosis.

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