Hypoxia-regulated miR-103-3p/FGF2 axis in adipose-derived stem cells promotes angiogenesis by vascular endothelial cells during ischemic tissue repair.
Lu Y., Cha D., Li Z., Xiao L., Liao X., Li S.
Animal Study on Chronic Wound, published in Int J Cardiol (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
- Int J Cardiol (2025)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39864666
- DOI
- 10.1016/j.ijcard.2025.133004
Abstract (original English)
Background Identifying factors mediating adipose-derived stem cells (ADSCs)-induced endothelial cell angiogenesis in hypoxic skin flap tissue is critical for reconstruction. While the paracrine action of VEGF by adipose-derived stem cells (ADSCs) is established in promoting endothelial cell angiogenesis, the role of FGF2 and its regulatory mechanisms in ADSCs paracrine secretion remains unclear. Methods We induced hypoxia and examined the expression level of FGF2 in ADSCs using ELISA, qRT-PCR, and western blotting. Proliferation of ADSCs under hypoxia was assessed using a CCK-8 assay. Co-culture experiments of hypoxia-induced ADSCs with vascular endothelial cells were conducted, and migration and tube formation abilities were evaluated through wound healing assays, transwell cell migration, and tube formation experiments. Results Hypoxia treatment induced significant upregulation of FGF2 expression in ADSCs, along with enhanced cell proliferation. Co-culture of hypoxia-induced ADSCs with vascular endothelial cells showed increased migration and tube formation abilities of endothelial cells. Knockdown of FGF2 inhibited these processes, while overexpression of miR-103-3p mimics in ADSCs suppressed endothelial cell migration and tube formation. FGF2 is a direct target of miR-103-3p in ADSCs. miR-103-3p/FGF2 axis regulates ADSCs on the biological activity of co-cultured vascular en
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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