ArticleStem cell research & therapy2023
Odontoblasts release exosomes to regulate the odontoblastic differentiation of dental pulp stem cells.
Article in Stem cell research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Extracellular vesicle therapies in regenerative endodontic procedures: A systematic review and meta-analysis of in vivo studies.Science progressPooled it
- Plasma exosome lncRNA panel as a non-invasive biomarker for molecular diagnosis of systemic lupus erythematosus.Clinical and experimental medicine · 2026Article
- Extracellular vesicles modulate skin aging biomarkers in a 3D reconstructed full-thickness skin model.Frontiers in cell and developmental biology · 2026Article
- Mechanistic insights into dental stem cells-derived exosomes in regenerative endodontics.International endodontic journal · 2025Review
- Isolation methods of exosomes derived from dental stem cells.International journal of oral science · 2025Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundDental pulp stem cells (DPSCs) play a crucial role in dentin-pulp complex regeneration. Further understanding of the mechanism by which DPSCs remain in a quiescent state could contribute to improvements in the dentin-pulp complex and dentinogenesis.
methodsTSC1 conditional knockout (DMP1-Cre+; TSC1
resultsOur study showed that mTORC1 activation in odontoblasts resulted in thicker dentin and higher dentin volume/tooth volume of molars, and it increased the expression levels of the exosome markers CD63 and Alix. In vitro, when DPSCs were cocultured with MDPC23 cells, odontoblastic differentiation was inhibited. However, the inhibition of odontoblastic differentiation was reversed when DPSCs were cocultured with MDPC23 cells with mTORC1 overactivation. To further study the effects of mTORC1 on exosome release from odontoblasts, MDPC23 cells were treated with rapamycin or shRNA-TSC1 to inactivate or activate mTORC1, respectively. The results revealed that exosome release from odontoblasts was negatively correlated with mTORC1 activity. Moreover, exosomes derived from MDPC23 cells with active or inactive mTORC1 inhibited the odontoblastic differentiation of DPSCs at the same concentration. miRNA sequencing analysis of exosomes that were derived from shTSC1-transfected MDPC23 cells, rapamycin-treated MDPC23 cells or nontreated MDPC23 cells revealed that the majority of the miRNAs were similar among these groups. In addition, exosomes derived from odontoblasts inhibited the odontoblastic differentiation of DPSCs, and the inhibitory effect was positively correlated with exosome concentration.
conclusionmTORC1 regulates exosome release from odontoblasts to inhibit the odontoblastic differentiation of DPSCs, but it does not alter exosomal contents. These findings might provide a new understanding of dental pulp complex regeneration.
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Registered trials
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