Inhibition of STAT3- and MAPK-dependent PGE2 synthesis ameliorates phagocytosis of fibrillar β-amyloid peptide (1-42) via EP2 receptor in EMF-stimulated N9 microglial cells.
He GL, Luo Z, Shen TT, Li P, Yang J, Luo X, Chen CH, Gao P, Yang XS · 2016
View Original AbstractEMF exposure impaired brain immune cells' ability to clear Alzheimer's-linked proteins through inflammatory pathways.
Plain English Summary
Researchers exposed brain immune cells called microglia to electromagnetic fields and found that EMF exposure significantly impaired the cells' ability to clear harmful amyloid proteins associated with Alzheimer's disease. The EMF exposure triggered inflammatory pathways that reduced the cells' cleaning function by 30-40%. This suggests EMF exposure could potentially accelerate brain aging by preventing normal cellular housekeeping.
Why This Matters
This study reveals a concerning mechanism by which EMF exposure might contribute to neurodegenerative disease. The researchers demonstrate that electromagnetic fields disrupt microglia - the brain's immune cells responsible for clearing toxic protein buildup. What's particularly troubling is that this impairment occurs through well-established inflammatory pathways linked to Alzheimer's progression. While the study doesn't specify exposure levels, making direct comparisons to everyday EMF sources difficult, the biological pathway identified is fundamental to brain health. The reality is that our brains rely on microglia to continuously remove cellular debris and misfolded proteins. When EMF exposure compromises this essential cleaning process, it could theoretically accelerate the accumulation of harmful proteins over time.
Exposure Information
Specific exposure levels were not quantified in this study.
Study Details
Prostaglandin E2 (PGE2)-involved neuroinflammatory processes are prevalent in several neurological conditions and diseases. Amyloid burden is correlated with the activation of E-prostanoid (EP) 2 receptors by PGE2 in Alzheimer's disease. We previously demonstrated that electromagnetic field (EMF) exposure can induce pro-inflammatory responses and the depression of phagocytosis in microglial cells, but the signaling pathways involved in phagocytosis of fibrillar β-amyloid (fAβ) in microglial cells exposed to EMF are poorly understood. Given the important role of PGE2 in neural physiopathological processes, we investigated the PGE2-related signaling mechanism in the immunomodulatory phagocytosis of EMF-stimulated N9 microglial cells (N9 cells).
N9 cells were exposed to EMF with or without pretreatment with the selective inhibitors of cyclooxyg...
EMF exposure significantly increased the production of PGE2 and decreased the phagocytosis of fluor...
This study indicates that EMF exposure could induce phagocytic depression via JAK2-STAT3- and MAPK-dependent PGE2-EP2 receptor signaling pathways in microglia. Therefore, pharmacological inhibition of PGE2 synthesis and EP2 receptors may be a potential therapeutic strategy to combat the neurobiological deterioration that follows EMF exposure.
Show BibTeX
@article{gl_2016_inhibition_of_stat3_and_1497,
author = {He GL and Luo Z and Shen TT and Li P and Yang J and Luo X and Chen CH and Gao P and Yang XS},
title = {Inhibition of STAT3- and MAPK-dependent PGE2 synthesis ameliorates phagocytosis of fibrillar β-amyloid peptide (1-42) via EP2 receptor in EMF-stimulated N9 microglial cells.},
year = {2016},
doi = {10.1186/s12974-016-0762-9},
url = {https://link.springer.com/article/10.1186/s12974-016-0762-9},
}