Objectives: Mitophagy is an important mitochondrial quality control mechanism. In this study, we investigated the mitochondrial damage and mitophagy occurred in inflammatory human dental pulp and lipopolysaccharide-stimulated preodontoblasts.
Materials and methods: In dental pulp tissues and lipopolysaccharide-stimulated preodontoblasts, immunofluorescences and Western blot were performed to detect the expression of mitochondrial and mitophagy-related proteins, and autophagy markers were also examined. Reactive oxygen species generated by mitochondria were examined by MitoSOX. Transmission electron microscope (TEM) was used to examine the morphology of mitochondria in lipopolysaccharide-stimulated preodontoblasts.
Results: The active fission activity of mitochondria and mitophagy in inflammatory dental pulp was observed. In lipopolysaccharide-treated preodontoblasts, mitophagy-related proteins were also upregulated. Moreover, increased reactive oxygen species in the inflamed preodontoblasts were observed. Additionally, single-membrane autolysosomes containing partially degraded mitochondria with swollen inner membranes in lipopolysaccharide-treated preodontoblasts were observed by TEM.
Conclusions: These results indicate that mitochondria were damaged and mitophagy might be activated to degrade impaired mitochondria in inflamed odontoblasts.
Keywords: PINK1; Parkin; inflammation; lipopolysaccharide; mitochondria; preodontoblast.
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