MSC-derived small extracellular vesicles promote dental pulp repair by alleviating inflammation in pulpitis via AKT and p38 MAPK pathways

Clicks: 8
ID: 320369
2026
Article Quality & Performance Metrics
Overall Quality
0.0 /100
Combines engagement data with AI-assessed academic quality
AI Quality Assessment
Not analyzed
Abstract
BACKGROUND: Pulpitis compromises dental pulp defense and repair, and current therapies inadequately resolve inflammation. Mesenchymal stem/stromal cell (MSC)-derived small extracellular vesicles (sEVs) exhibit potent anti-inflammatory properties, yet their protective role in inflamed dental pulp and underlying mechanisms remain unclear. This study aimed to evaluate the therapeutic potential of MSC-sEVs in experimental rat pulpitis, define the contribution of sEV-associated CD73 activity, and elucidate the molecular mechanisms by which MSC-sEVs attenuate lipopolysaccharide (LPS)-induced inflammatory responses in dental pulp cells (DPCs). METHODS: sEVs were enriched from human MSC-conditioned medium by size-based fractionation and characterized for particle size, protein concentration, and CD73/ecto-5՛-nucleotidase (NT5E) activity. Rat pulpitis was induced by LPS application to Class I cavities of maxillary molars. In vitro inflammation was modeled using LPS-stimulated DPC spheroids. Inflammatory mediators were quantified by nitric oxide (NO) quantification and enzyme-linked immunosorbent assay (ELISA), while signaling pathways were examined by Western blotting and pharmacological inhibition of CD73, adenosine receptors, AKT, ERK, and p38 MAPK. RESULTS: MSC-sEVs significantly alleviated pulpal inflammation and promoted reparative dentin formation in vivo, with efficacy comparable to mineral trioxide aggregate (MTA). In LPS-stimulated DPC spheroids, MSC-sEVs suppressed pro-inflammatory and nociceptive mediator release. Mechanistically, MSC-sEVs reduced NO, IL-6, MMP9, and NGF production through a CD73-adenosine receptor-dependent pathway involving AKT activation and p38 MAPK inhibition, but not ERK signaling. CONCLUSIONS: MSC-sEVs promote dental pulp repair by modulating inflammation through a CD73-mediated adenosine signaling axis, highlighting their potential as a cell-free therapeutic for early pulpitis intervention.
Reference Key
openalex_W7167831781 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors J Y Shi, Yuanyuan Jiang, Shipin Zhang, Annie Shrestha, Xiaoli Hu, Lu Jiang, Wei Seong Toh
Journal stem cells international
Year 2026
DOI
10.1093/stmcls/sxag038
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.