miR-296-5p promotes autophagy in mouse LS8 cells under excessive fluoride via AMPK/ULK1 pathways

Numerous microRNAs participate in regulating the pathological process of autophagy. We have found miR296-5p is one of the most significantly down-regulated microRNAs in a high concentration of sodium fluoride. However, it is not clear whether miR-296-5p augments autophagy in dental fluorosis. Our purpose is to explore the function of miR-296-5p in regulating autophagy of excessive fluoride development. Thus, the cell line of ameloblasts LS8 was exposed to a 1.5 mM dose of NaF and miR-296-5p-mimics, Real-time qPCR, CCK-8 assays, Fluorescence imaging and Western blot analysis were performed. Autophagy was observed. As our results indicated, miR-296-5p overexpression in mouse LS8 cells significantly accelerated autophagy. The autophagy inhibition effect of miR-296-5p underexpression was consistent with the effect of the AMPK inhibitor. And we found that the expression of LC3II was decreased via down-regulation of AMPK. The change of ULK1 by miR296-5p may be accomplished through AMPK. Thus, miR-296-5p may improve the secretion of autophagic mediators by activating AMPK/ULK1 expression in fluorosis, suggesting that miR-296-5p, AMPK/ULK1 may be potential therapeutic targets under the higher fluoride stimulation.

Automated summary

This study found that overexpression of miR-296-5p can accelerate autophagy in fluoride-induced dental fluorosis, while its underexpression has an inhibitory effect on autophagy. MiR-296-5p may improve the secretion of autophagic mediators by activating AMPK/ULK1 expression, suggesting it as a potential therapeutic target under high fluoride stimulation.