ArticleStem cell research & therapy2025
Human dental follicle stem cell-derived exosomes reduce root resorption by inhibiting periodontal ligament cell pyroptosis.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Dysregulation of miR-140-3p is involved in the pathogenesis of pulpitis via the regulation of ACSL1.Odontology · 2026Article
- proBDNF-SorCS2 Axis Suppresses Osteogenesis and Augments Inflammation of Human Periodontal Ligament Stem Cells in Inflammatory Conditions.International dental journal · 2026Article
- Cell Death in Orthodontic Tooth Movement: Recent Advances and Emerging Insights.International journal of molecular sciences · 2026Review
- MicroRNAs in periodontal disease: from pathogenic mechanisms and RANKL/OPG regulation to nanoparticle delivery and personalized medicine.Frontiers in immunology · 2026Review
- Advances in understanding exosome-mediated regulation of macrophage function.Frontiers in immunology · 2026Review
- Decoding the molecular mechanisms of pyroptosis and its therapeutic development prospects.Frontiers in cell and developmental biology · 2026Review
- Diagnostic and therapeutic potential of oral cavity-derived exosomes in oral and maxillofacial tissue engineering: current advances and future perspectives.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The role of stem cell-derived exosomes in regulating pyroptosis for disease therapy.Stem cell research & therapy · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundTo explore the therapeutic effects and mechanisms of the exosomes derived from dental follicle stem cells (DFSC-Exos) in reducing osteoclastogenesis and root resorption (RR) by inhibiting periodontal ligament cell (PDLC) pyroptosis.
methodsDFSC-Exos, with force stimulation (Force-Exos) or without (Ctrl-Exos), were co-cultured with human PDLCs in vitro and injected into the periodontal ligament (PDL) of rats following the establishment of RR models in vivo. Subsequently, resorption volume, PDLC pyroptotic ratio, and NLRP3-mediated pyroptosis pathway activation were performed to investigate the therapeutic effects of DFSC-Exos on PDLC pyroptosis during RR. Furthermore, the number of M1/M2 macrophages, osteoclast formation, and transwell polarization elucidated the role of Force-Exo treatment in macrophage polarization and osteoclastogenesis by inhibiting pyroptosis. Exosomal miRNA sequencing and bioinformatic analysis were used to identify differentially abundant exosome-derived miRNAs, as well as the dominant biological processes and pathways modulated by miRNA. The administration of miRNA inhibitors further verified the regulation of exosomal miRNA on RR via modulating pyroptosis. Moreover, the potential mechanisms involving candidate miRNAs and relevant pathways were explored.
resultsExosomes released by force-stimulated DFSCs (Force-Exos) inhibited NOD-like receptor 3 (NLRP3)-mediated PDLC pyroptosis, which impacted M1 macrophage activation and osteoclast formation. Based on exosomal miRNA sequencing, miR-140-3p in Force-Exos were transferred to PDLCs, and the administration of miR-140-3p inhibitors significantly reversed the reduction in PDLC pyroptosis, M1 macrophage polarization, osteoclast number, and resorption volume caused by Force-Exos. More importantly, mechanistic studies demonstrated that miR-140-3p mediated the function of Force-Exos by targeting DNA methyltransferase 1 (DNMT1) to alter the DNA methylation of suppressor of cytokine signaling (SOCS1) and the downstream nuclear factor κB (NF-κB) signaling pathway in PDLCs. Blocking the DNMT1/SOCS1/NFκB axis with DFSC-derived exosomal miR-140-3p downregulated NLRP3-mediated PDLC pyroptosis to impact M1 polarization and osteoclast formation, thereby alleviating RR.
conclusionDFSC-Exos downregulated NLRP3-mediated PDLC pyroptosis via miR-140-3p to block DNMT1/SOCS1/NFκB axis, which impacted M1 polarization and osteoclast formation, thereby alleviating RR.
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