Small EVs From Adipose-Derived MSCs Modulate Epidermal Barrier and Inflammation Via Sphingosine-1-Phosphate Signaling Pathway.
Shin KO., Lee JH., Chae S., Goto K., An H., Wakefield JS.
Animal Study, published in J Extracell Vesicles (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
- J Extracell Vesicles (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40693579
- DOI
- 10.1002/jev2.70121
Abstract (original English)
Epidermal permeability barrier defects are associated with several skin diseases, including atopic dermatitis (AD). Using an AD mouse model, we previously demonstrated that topically administered small extracellular vesicles (sEVs) (prepared following the International Society of Extracellular Vesicles recommendations) from human adipose tissue-derived mesenchymal stem cells (ASC) ameliorate skin inflammation and normalize barrier function in parallel with increased ceramide (a key barrier lipid) production. To elucidate how ASC-sEVs alleviate these AD skin abnormalities, we characterized lipids and ceramide metabolic enzymes in ASC-sEVs versus donor ASCs. Our study revealed that free fatty acid, ceramide, and sphingomyelin are enriched in ASC-sEVs versus donor ASCs, while the synthetic enzymes of ceramide (and acidic sphingomyelinase), and sphingosine-1-phosphate (sphingosine kinase) are significantly higher in ASC-sEVs versus donor ASCs. Conversely, ceramide (ceramidase), and sphingosine-1-phosphate hydrolytic enzymes (sphingosine-1-phosphate lyase and sphingosine-1-phosphate phosphatase) are lower in ASC-sEVs, suggesting that ceramide and sphingosine-1-phosphate levels could elevate in cells that receive ASC-sEVs. ASC-sEV-mediated increases in sphingosine-1-phosphate suppress pro-inflammatory cytokine production in AD-model human keratinocytes. Additionally, keratinocyte dif
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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