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Exosome Derived From Human Umbilical Cord Mesenchymal Stem Cell Mediates MiR-181c Attenuating Burn-induced Excessive
Xiao Li1, Lingying Liu1, Jing Yang1
1Department of Burn & Plastic Surgery, The First Affiliated Hospital to PLA General Hospital, Beijing 100048, China.
Abstract:
Mesenchymal stem cell (MSC)-derived exosomes have diverse functions in regulating wound healing and inflammation; however, the molecular mechanism of human umbilical cord MSC (hUCMSC)-derived exosomes in regulating burn-induced inflammation is not well understood. We found that burn injury significantly increased the inflammatory reaction of rats or macrophages exposed to lipopolysaccharide (LPS), increased tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) levels and decreased IL-10 levels. hUCMSC-exosome administration successfully reversed this reaction. Further studies showed that miR-181c in the exosomes played a pivotal role in regulating inflammation. Compared to control hUCMSC-exosomes, hUCMSC-exosomes overexpressing miR-181c more effectively suppressed the TLR4 signaling pathway and alleviated inflammation in burned rats. Administration of miR-181c-expressing hUCMSC-exosomes or TLR4 knockdown significantly reduced LPS-induced TLR4 expression by macrophages and the inflammatory reaction. In summary, miR-181c expression in hUCMSC-exosomes reduces burn-induced inflammation by downregulating the TLR4 signaling pathway.
Insights
Human umbilical cord mesenchymal stem cell (hUCMSC)-derived exosomes reduce burn inflammation. Exosomes containing miR-181c suppress the TLR4 pathway, decreasing inflammatory markers and improving healing in rats.
Area of Science:
- Biomedical Engineering
- Regenerative Medicine
- Immunology
Background:
- Mesenchymal stem cell (MSC)-derived exosomes modulate wound healing and inflammation.
- The precise molecular mechanisms of human umbilical cord MSC (hUCMSC)-derived exosomes in burn inflammation remain unclear.
Purpose of the Study:
- To elucidate the role of hUCMSC-derived exosomes in regulating burn-induced inflammation.
- To investigate the specific molecular pathways and microRNAs involved.
Main Methods:
- Burn injury model in rats and lipopolysaccharide (LPS)-stimulated macrophages.
- Administration of hUCMSC-derived exosomes, including those overexpressing miR-181c.
- Analysis of inflammatory cytokine levels (TNF-α, IL-1β, IL-10) and TLR4 signaling pathway activation.
Main Results:
- Burn injury and LPS exposure significantly increased pro-inflammatory cytokines (TNF-α, IL-1β) and decreased anti-inflammatory IL-10.
- hUCMSC-exosome administration reversed these inflammatory changes.
- miR-181c within exosomes was identified as a key regulator, effectively suppressing the TLR4 pathway and reducing inflammation in burned rats.
Conclusions:
- hUCMSC-derived exosomes mitigate burn-induced inflammation.
- miR-181c plays a critical role by downregulating the TLR4 signaling pathway.
- These findings highlight the therapeutic potential of hUCMSC-exosomes for managing burn-related inflammatory conditions.
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