Adipose mesenchymal stem cell exosomes promote wound healing through accelerated keratinocyte migration and proliferation by activating the AKT/HIF-1α axis.
Zhang Y., Han F., Gu L., Ji P., Yang X., Liu M.
Animal Study on Chronic Wound, Chronic Inflammation, published in J Mol Histol (2020) — 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
- J Mol Histol (2020)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 32556903
- DOI
- 10.1007/s10735-020-09887-4
Abstract (original English)
Accelerating wound healing is a key consideration for surgeons. The three stages of wound healing include the inflammatory response, cell proliferation and tissue repair, and much research has focused on the migration and proliferation of epidermal cells, since this is one of the most important steps in wound healing. Studies have shown that adipose mesenchymal stem cells (ADSCs) can promote wound healing by releasing exosomes, although the specific mechanism remains unclear. To clarify the role of adipose mesenchymal stem cell exosomes (ADSCs-exo), we constructed a HaCaT cells model and a mouse wound healing model to examine the effects of ADSCs-exo on wound healing. CCK8 assays and the scratch test showed that ADSCs-exo could promote the proliferation and migration of HaCaT cells. Western blotting and real-time PCR showed that ADSCs-exo upregulated the phosphorylation of AKT and the expression of HIF-1α in HaCaT cells. HIF-1α expression was reduced by inhibiting AKT phosphorylation,and the migration of HaCaT cells simultaneously slowed. These results were also confirmed in vivo. In conclusion, we confirmed that ADSCs-exo promote the proliferation and migration of HaCaT cells by regulating the activation of the AKT/HIF-1α signaling pathway, thus promoting wound healing.
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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