Conclusion
This study demonstrated that BRF1 promoted autophagy activation and odontogenic differentiation in pulpitis.
Methods
Immunohistochemical analysis was used to examine BRF1 expression, autophagy levels, and dentinogenic markers in normal and inflamed pulp. The presence of autophagosomes was observed by transmission electron microscopy. Primary hDPSCs were treated with 1 μg/mL lipopolysaccharide (LPS) for different lengths of time. The expression of BRF1 and autophagy makers was determined by Western blotting. BRF1 knockdown and 3 MA treatment were employed to assess changes in autophagy and dentinogenic differentiation. Double immunofluorescence staining was performed to co-localize BRF1 with LC3B in pulp tissue.
Objective
While post-transcriptional modifications play a pivotal role in the autophagy regulation, studies on dental pulp disease are limited. This study investigated the effect of BRF1 on autophagy in inflamed pulp tissue and human dental pulp stem cells (hDPSCs).
Results
The expressions of BRF1, LC3, DMP1, and DSP were significantly elevated in the inflamed pulp. LPS enhanced the protein production of IL-6, BRF1, LC3, and Beclin-1 from 6 h to 24 h after the treatment. BRF1 knockdown reduced the ratio of LC3-II/LC3-I and the differentiation ability of hDPSCs, while 3 MA inhibited LPS-mediated dentinogenic differentiation. Double-labeling revealed that BRF1 co-localized with LC3B in inflamed pulp.