Exosomes of human adipose stem cells mitigate irradiation injury to salivary glands by inhibiting epithelial-mesenchymal transition through miR-199a-3p targeting Twist1 and regulating TGFβ1/Smad3 pathway.
Guo X., Huang Z., Wu F., Jiang W., Li Y., Wang T.
Animal Study, published in Theranostics (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Theranostics (2025)
- Country
- Australia
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39897544
- PMCID
- PMC11780531
- DOI
- 10.7150/thno.102346
- Citations
- 9
Abstract (original English)
Rationale: Currently, irradiation-injured salivary glands (IR-SG) lack effective clinical treatment options. Emerging treatments using exosomes (Exo) have shown promising outcomes for various diseases. However, the efficacy of exosome in treating IR-SG remains unexplored. This study aimed to use exosomes to restore IR-SG function and to explore their underlying mechanisms. Methods: Exosomes isolated from human adipose-derived stem cell (ADSC-Exo) were injected into C57BL/6 mice that had their salivary glands injured with 14Gy. RNA sequencing profiled differentially expressed miRNAs and mRNAs of IR-SG. Epithelial-mesenchymal transition (EMT) mechanisms were further examined using SMG-C6 cells. Results: Exo-treated mice had a 96% increase in saliva secretion, higher cell proliferation, upregulated tissue repair/regeneration genes, and preserved functional cells with fewer collagen fibers compared to saline-treated mice. Exo treatment increased the expression of epithelial cell markers while decreasing mesenchymal cell markers. Notably, miR-199a-3p was significantly upregulated in Exo-treated mice, promoting cell growth and reducing EMT. Twist1, an EMT transcription factor, was identified as a direct target of miR-199a-3p and confirmed by luciferase assays. Twist1 overexpression promoted EMT, but Exo treatment or Twist1 knockdown reduced EMT marker expression and inactivated the T
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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