Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

Exosomes derived from adipose tissue-derived stem cells alleviated H 2 O 2 -induced oxidative stress and endothelial-to-mesenchymal transition in human umbilical vein endothelial cells by inhibition of the mir-486-3p/Sir

Li Y., Xiao Y., Shang Y., Xu C., Han C., Hu D.

Animal Study on Scar, published in Cell Biol Toxicol (2024) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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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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
Cell Biol Toxicol (2024)
Country
Switzerland
Reported sample size
—
Source database
PubMed
PMID
38789630
PMCID
PMC11126451
DOI
10.1007/s10565-024-09881-6
Citations
14

Abstract (original English)

Hypertrophic scar (HS) is characterized by excessive collagen deposition and myofibroblasts activation. Endothelial-to-mesenchymal transition (EndoMT) and oxidative stress were pivotal in skin fibrosis process. Exosomes derived from adipose tissue-derived stem cells (ADSC-Exo) have the potential to attenuate EndoMT and inhibit fibrosis. The study revealed reactive oxygen species (ROS) levels were increased during EndoMT occurrence of dermal vasculature of HS. The morphology of endothelial cells exposure to H 2 O 2, serving as an in vitro model of oxidative stress damage, transitioned from a cobblestone-like appearance to a spindle-like shape. Additionally, the levels of endothelial markers decreased in H 2 O 2 -treated endothelial cell, while the expression of fibrotic markers increased. Furthermore, H 2 O 2 facilitated the accumulation of ROS, inhibited cell proliferation, retarded its migration and suppressed tube formation in endothelial cell. However, ADSC-Exo counteracted the biological effects induced by H 2 O 2 . Subsequently, miRNAs sequencing analysis revealed the significance of mir-486-3p in endothelial cell exposed to H 2 O 2 and ADSC-Exo. Mir-486-3p overexpression enhanced the acceleration of EndoMT, its inhibitors represented the attenuation of EndoMT. Meanwhile, the target regulatory relationship was observed between mir-486-3p and Sirt6, whereby Sirt6 exerted it

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.

How we grade evidence
AnimalsHumansAdipose TissueCell MovementCell ProliferationEpithelial-Mesenchymal TransitionExosomesHuman Umbilical Vein Endothelial CellsHydrogen PeroxideMicroRNAs

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