Human-induced pluripotent stem cell derived exosomal miR-103a-3p accelerate urethral injury recovery by promoting angiogenesis via TGFBR3/VEGF/FAK axis
Sun F., Liu H., Zhang D., Ding G., Chi Y., Wang J.
Animal Study on Hip, published in 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
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- Study type
- Animal Study
- Journal
- Stem Cell Res Ther (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41691299
- PMCID
- PMC13011571
- DOI
- 10.1186/s13287-026-04939-0
Abstract (original English)
Background Vascular dysfunction caused by urethral injury often leads to delayed repair. Exosome from stem cell showed promise in tissue regeneration. But human induced pluripotent stem cell-derived exosomes (hiPSC-Exo) has not been reported the angiogenesis ability in urethral injury repair and their potential mechanisms. Method The exosome was extracted from hiPSCs. The in vivo and in vitro experiments were performed to investigate the effects of hiPSC-Exo on angiogenesis. The miRNA-seq bioinformatics, luciferase assay and related functional experiments were performed to determine potential mechanism. Result Exosome was extracted from hiPSCs by ultracentrifugation. Compared to the control group, hiPSC-Exo significantly promoted blood flow supply to the ischemic lower limbs of mice and rat model of urethral defects to accelerate injury repair. We found that hiPSC-Exo significantly enhanced the proliferation, migration, and tube formation ability of endothelial cells in vitro. MiRNA-seq analysis and experiments verified that miR-103a-3p was highly expressed in HUVEC treated with hiPSC-Exo and significantly enhanced the proliferation, migration, invasion, and angiogenesis effects. TGFBR3 was identified as a direct target of miR-103a-3p through bioinformatics, qPCR, and dual luciferase assays. Overexpression of TGFBR3 leaded to reduced proliferative, migrative and angiogenesis ab
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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