The effect of inhibiting exosomes derived from adipose-derived stem cells via the TGF-β1/Smad pathway on the fibrosis of keloid fibroblasts.
Wu ZY., Zhang HJ., Zhou ZH., Li ZP., Liao SM., Wu ZY.
Laboratory Study on Scar, published in Gland Surg (2021) — 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
- Laboratory Study
- Journal
- Gland Surg (2021)
- Country
- China (Republic : 1949- )
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 33842249
- PMCID
- PMC8033055
- DOI
- 10.21037/gs-21-4
- Citations
- 32
Abstract (original English)
The main mechanism of keloid formation is that keloid fibroblasts (KFs) apoptosis is inhibited, leading to excessive proliferation. Transforming growth factor-β1 (TGF-β1) is a key signal molecule in the process of regulating cell fibrosis. This paper discusses the effect of adipose-derived stem cell exosomes (ADSCs-EXO) on the proliferation and apoptosis of KFS and its possible mechanism, in order to provide reference for the clinical intervention of hypertrophic scar. ADSCs were isolated and cultured from human adipose tissue, the supernatant was collected, and the exosomes secreted by ADSCs-EXO were extracted by ultracentrifugation. At the same time, KFs were cultured from human keloid tissue to P3 generation, and then divided into four groups: control group, experimental group A, experimental group B and experimental group C. KFs were then cultured with four concentrations of ADSCs-EXO (0, 1, 10, and 100 µg/mL, respectively). After 24 hours, cells in each group were taken to detect the following: proliferation of cells in each group using the cell counting Kit 8 (CCK-8) method, cell migration ability via the Transwell test, cell apoptosis by flow cytometry, collagen synthesis using the hydroxyproline method, messenger ribonucleic acid (mRNA) expression of fibrosis-related genes in each group by real-time fluorescent polymerase chain amplification, and the expression of fibro
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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