Multiple Doses of Overexpression of Cellular Prion Protein in Adipose-derived Mesenchymal Stem Cells Safely Provided Additional Protection to the Lungs Against Bleomycin-induced Damage in Rodents.
Lin KC., Yeh JN., Chen YL., Chiang JY., Huang CR., Wang YT.
Animal Study, published in Curr Stem Cell Res Ther (2026) — 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
- Curr Stem Cell Res Ther (2026)
- Country
- United Arab Emirates
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42136464
- DOI
- 10.2174/011574888X416268251210125540
Abstract (original English)
Introduction We tested whether early administration of multiple doses of adipose-derived mesenchymal stem cells (ADMSCs) overexpressing cellular prion protein (PrPC-OVE) could preserve lung parenchyma and function in a rodent model of bleomycin-induced pulmonary fibrosis (PF). Methods Cell culture, immunohistochemistry, immunofluorescence, and western blot analyses were conducted. Animals were categorized into sham-control (Group 1), PF (Group 2), PF + ADMSCs (one dose; Group 3), PF + ADMSCs (three doses; Group 4), PF + PrPC-OVE in ADMSCs (one dose; Group 5), and PF + PrPC-OVE in ADMSCs (three doses; Group 6). Results In vitro, bleomycin suppressed L2 cell proliferation and increased apoptosis and epithelial-mesenchymal transition (EMT) markers, which were significantly reversed by ADMSCs and further enhanced by PrPC-OVE in ADMSCs. TGF-β/Smads signaling-mediated EMT was identified as a crucial mechanism in cellular fibrosis and PF, which was significantly suppressed by silencing TGF-β in L2 cells and PrPC-OVE in ADMSCs co-cultures and lung tissue. By days 28 and 42 after PF induction, O₂ saturation (%) was highest in Group 1, lowest in Group 2, and notably higher in Group 6 than in Groups 3-5. Right-ventricular (RV) systolic blood pressure showed an inverse trend. RV and left lung weights-to-tibial length ratios were significantly greater in Group 2 at both time points. By day
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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