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Exosomes Derived from Human Amniotic Fluid Mesenchymal Stem Cells Preserve Microglia and Neuron Cells from Aβ
Manuela Zavatti1, Martina Gatti1, Francesca Beretti1
1Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy.
Background:
Neuroinflammation is involved in neuronal cell death that occurs in neurodegenerative diseases such as Alzheimer's disease (AD). Microglia play important roles in regulating the brain amyloid beta (Aβ) levels, so immunomodulatory properties exerted by mesenchymal stem cells may be exploited to treat this pathology. The evidence suggests that the mechanism of action of human amniotic fluid stem cells (hAFSCs) is through their secretome, which includes exosomes (exo).
Methods:
We examined the effect of exosomes derived from human amniotic fluid stem cells (hAFSCs-exo) on activated BV-2 microglia cells by lipopolysaccharide (LPS) as a neuroinflammation model. To investigate the exo effect on the interplay between AD neurons and microglia, SH-SY5Y neuroblastoma cells treated with Aβ were exposed to a conditioned medium (CM) obtained from activated BV-2 or co-culture systems.
Results:
We found that the upregulation of the markers of pro-inflammatory microglia was prevented when exposed to hAFSC-exo whereas the markers of the anti-inflammatory macrophage phenotype were not affected. Interestingly, the hAFSC-exo pretreatment significantly inhibited the oxidative stress rise and apoptosis occurring in the neurons in presence of both microglia and Aβ.
Conclusion:
We demonstrated that hAFSC-exo mitigated an inflammatory injury caused by microglia and significantly recovered the neurotoxicity, suggesting that hAFSC-exo may be a potential therapeutic agent for inflammation-related neurological conditions, including AD.
Insights
Human amniotic fluid stem cell-derived exosomes (hAFSC-exo) reduce neuroinflammation and protect neurons from amyloid beta (Aβ)-induced toxicity. These findings suggest hAFSC-exo as a promising therapeutic for Alzheimer
Area of Science:
- Neuroscience
- Immunology
- Stem Cell Biology
Background:
- Neuroinflammation contributes to neuronal death in neurodegenerative diseases like Alzheimer's disease (AD).
- Microglia modulate amyloid beta (Aβ) levels, and mesenchymal stem cells possess immunomodulatory properties.
- Human amniotic fluid stem cells (hAFSCs) exert effects via their secretome, including exosomes (exo).
Purpose of the Study:
- To investigate the therapeutic potential of exosomes derived from human amniotic fluid stem cells (hAFSCs-exo) in a neuroinflammation model.
- To assess the impact of hAFSCs-exo on microglia activation and neuronal survival in the context of Alzheimer's disease pathology.
Main Methods:
- Exosomes from hAFSCs (hAFSCs-exo) were applied to lipopolysaccharide (LPS)-activated BV-2 microglia cells.
- SH-SY5Y neuroblastoma cells treated with Aβ were exposed to conditioned medium from activated BV-2 cells or co-culture systems to model AD neuroinflammation.
- The effects of hAFSCs-exo on inflammatory markers, oxidative stress, and apoptosis were analyzed.
Main Results:
- hAFSCs-exo prevented the upregulation of pro-inflammatory microglia markers.
- hAFSCs-exo did not significantly affect anti-inflammatory macrophage phenotype markers.
- Pretreatment with hAFSCs-exo inhibited oxidative stress and apoptosis in neurons exposed to microglia and Aβ.
Conclusions:
- hAFSCs-exo mitigate microglial-induced inflammatory injury.
- hAFSCs-exo significantly ameliorate neurotoxicity associated with inflammation and Aβ.
- hAFSCs-exo represent a potential therapeutic strategy for neurodegenerative conditions involving inflammation, such as AD.
