Hypoxic human adipose mesenchymal stem cells-derived extracellular vesicles induce P311 expression and inhibit activation and injury of human brain microvascular endothelial cells.
Zhang Y., Zhao H., Su Y., Yang S., Kang T., Li L.
Prospective Study on Face & Skin, published in Clin Hemorheol Microcirc (2025) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- 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
- Prospective Study
- Journal
- Clin Hemorheol Microcirc (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39973441
- DOI
- 10.1177/13860291241291326
Abstract (original English)
ObjectiveStem cell therapy can modify angiogenic pathways. Neural protein 3.1 (P311) possesses the pro-angiogenic property. This study strived to explore the action and mechanism of human adipose mesenchymal stem cells (hADSCs) in human brain microvascular endothelial cell (hBMEC) injury by regulating P311.MethodsThe hADSCs of the 3 rd passage were stained with oil red O, Alizarin red, and Alcian blue to assess adipogenic, osteogenic, and chondrogenic differentiation, followed by an analysis of immune phenotype via flow cytometry. After culturing hADSCs in hypoxic (5% oxygen) and normoxic (20% oxygen) conditions, extracellular vesicles (EVs) were extracted via ultracentrifugation, followed by morphology observation by microscopy, size distribution analysis via Nanoparticle tracking analysis, and surface marker determination by Western blot. hBMECs were treated with lipopolysaccharide (LPS) and cultured with normoxia or hypoxic hADSC-EVs. The effects of normoxia and hypoxic hADSC-EVs on proliferation, migration, and tube formation of hBMECs were assessed via CCK-8, Transwell, and tube formation assays. hBMECs were transfected with pcDNA3.0-P311 or P311 siRNA to evaluate the action of P311 on hBMEC injury.ResultsHypoxic hADSC-EVs had a larger mean diameter, a wider diameter distribution range, and a higher particle concentration than normoxic hADSC-EVs. Hypoxia and normoxic hADSC
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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