ArticleHeliyon2024
BRF1 promotes the odontogenic differentiation of dental pulp stem cells in pulpitis by inducing autophagy.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Long non-coding RNA FOXD2-AS1 promotes inflammation but suppresses osteogenesis in pulpitis via miR-338-3p/THBS1 axis.Odontology · 2026Article
- Long noncoding RNA NONRATT007487.2 drives cancer-induced bone pain progression through direct interaction with CXCL1.The Korean journal of pain · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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). 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. 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. Conclusion: This study demonstrated that BRF1 promoted autophagy activation and odontogenic differentiation in pulpitis.
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Registered trials
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