Exosomes from human adipose-derived mesenchymal stromal/stem cells accelerate angiogenesis in wound healing: implication of the EGR-1/lncRNA-SENCR/DKC1/VEGF-A axis.
Sun Y., Ju Y., Fang B.
Animal Study on Chronic Wound, published in Hum Cell (2022) — 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
- Hum Cell (2022)
- Country
- Japan
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 35751795
- DOI
- 10.1007/s13577-022-00732-2
Abstract (original English)
Exosomes (Exos) extracted from human adipose mesenchymal stromal/stem cells (hAD-MSCs) have been reported as therapeutic tools for tissue repair, but how they regulate angiogenesis of endothelial cells remains unknown. In this study, hAD-MSCs were isolated, and early growth response factor-1, Smooth muscle and endothelial cell enriched migration/differentiation-associated long-noncoding RNA (lncRNA-SENCR), and vascular endothelial growth factor-A (VEGF-A) overexpression or knockdown was achieved. Exos extracted from hAD-MSCs (hADSC-Exos) were co-cultured with human umbilical vein endothelial cells (HUVECs) to detect the effects of EGR-1, lncRNA-SENCR, and VEGF-A on angiogenesis and the relationships between EGR-1, lncRNA-SENCR, Dyskerin pseudouridine synthase 1 (DKC1), and VEGF-A. An in vivo experiment verified the effect of hADSC-Exos on the wound healing process. hADSC-Exos substantially promoted the proliferation, migration, and angiogenesis of HUVECs, which could be reversed by short-hairpin RNA SENCR (shSENCR) transfection. hADSC-Exos had elevated expression of EGR-1, which bound to the lncRNA-SENCR promoter. The suppressive effect of Exo-shEGR1 on HUVECs was counteracted by SENCR overexpression. LncRNA-SENCR was shown to interact with DKC1. Overexpression of DKC1 or lncRNA-SENCR maintained stable VEGF-A expression. Overexpression of VEGF-A reversed the suppressive effect
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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