Inhibitory effect of membrane‑free stem cell components derived from adipose tissues on skin inflammation in keratinocytes.
Ha SE., Vetrivel P., Kim SM., Bhosale PB., Kim HH., Pak JE.
Laboratory Study on Skin Aging, published in Mol Med Rep (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
- Laboratory Study
- Journal
- Mol Med Rep (2022)
- Country
- Greece
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 35169867
- DOI
- 10.3892/mmr.2022.12641
- Citations
- 3
Abstract (original English)
Inflammatory disorders of the skin are major public health concerns due to constant exposure to external stimuli. Skin cells are associated with prominent immune mechanisms to defend against adverse reactions. In the present study, the anti‑inflammatory properties of membrane‑free stem cell components (MFSCC) from adipose tissue‑derived stem cells (ADSCs) and their basic preventive effects on skin wrinkle formation using human keratinocytes (HaCaT) and fibroblast (Detroit 551) cells, were investigated. Initially, a human inflammation antibody array was used on tumor necrosis factor‑α (TNF‑α)/interferon‑γ (IFN‑γ)‑induced and MFSCC‑treated HaCaT cells. Array spots revealed three differential proteins, interleukin (IL)‑1 F1 (IL‑1α), IL‑6, and TIMP2. Of these three proteins, IL‑6 was significantly downregulated by MFSCC treatment. Western blot analysis revealed that IL‑6 and its key downstream proteins JAK2 and STAT3 were suppressed in MFSCC‑treated HaCaT cells. Further analysis revealed that MFSCC decreased the expression of TNF‑α/IFN‑γ‑induced phosphorylated (p)‑IκB‑α, p‑p65, p‑JNK, p‑ERK, and p‑p38 by inhibiting the activation of MAPK and NF‑κB pathways. Treatment of Detroit 551 cells with MFSCC increased COL1A1 and elastin but suppressed matrix metalloproteinase (MMP)‑1 and MMP‑8 protein expression levels. Collectively, these data indicated that MFSCC exhibited a primary inhibi
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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