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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Electromagnetic pulse activated brain microglia via the p38 MAPK pathway
Long-Long Yang1, Yan Zhou2, Wei-Dong Tian3
1Department of Radiation Biology, School of Public Health, Fourth Military Medical University, 169 Changle West Road, Xi'an, Shaanxi 710032, China; Department of Radiation Medicine, School of Public Health, Fourth Military Medical University, 169 Changle West Road, Xi'an, Shaanxi 710032, China.
Abstract:
Previously, we found that electromagnetic pulses (EMP) induced an increase in blood brain barrier permeability and the leakage of albumin from blood into brain tissue. Albumin is known to activate microglia cells. Thus, we hypothesised that microglia activation could occur in the brain after EMP exposure. To test this hypothesis, the morphology and secretory function of microglia cells, including the expression of OX-42 (a marker of microglia activation), and levels of TNF-α, IL-10, IL-1β, and NO were determined in the rat cerebral cortex after EMP exposure. In addition, to examine the signalling pathway of EMP-induced microglia activation, protein and phosphorylated protein levels of p38, JNK and ERK were determined. It was found that the expression of OX-42increased significantly at 1, 6 and 12h (p<0.05) and recovered to the sham group level at 24h after EMP exposure. Levels of NO, TNF-α and IL-10 also changed significantly in vivo and in vitro after EMP exposure. The protein level of p38 and phosphorylated p38 increased significantly after EMP exposure (p<0.05) and recovered to sham levels at 12 and 24h, respectively. Protein and phosphorylated protein levels of ERK and JNK did not change. SB203580 (p38 inhibitor) partly prevented the change in NO, IL-10, IL-1β, TNF-α levels induced by EMP exposure. Taken together, these results suggested that EMP exposure (200kV/m, 200 pulses) could activate microglia in rat brain and affect its secretory function both in vivo and in vitro, and the p38 pathway is involved in this process.
Insights
Electromagnetic pulse (EMP) exposure activates microglia cells in the rat brain, altering their function. The p38 signaling pathway is implicated in this EMP-induced microglia activation and subsequent inflammatory responses.
Area of Science:
- Neuroscience
- Immunology
- Biophysics
Background:
- Electromagnetic pulses (EMP) can increase blood-brain barrier permeability, leading to albumin leakage into brain tissue.
- Albumin is known to activate microglia, suggesting a potential link between EMP exposure and microglia activation.
Purpose of the Study:
- To investigate whether EMP exposure activates microglia in the rat brain.
- To examine the effects of EMP exposure on microglia morphology, secretory function, and associated signaling pathways.
Main Methods:
- Rats were exposed to EMP (200kV/m, 200 pulses).
- Microglia activation marker (OX-42) and cytokine levels (TNF-α, IL-10, IL-1β, NO) were measured.
- Protein and phosphorylated protein levels of p38, JNK, and ERK signaling pathways were analyzed.
- The effect of a p38 inhibitor (SB203580) on EMP-induced changes was assessed.
Main Results:
- EMP exposure significantly increased OX-42 expression, indicating microglia activation.
- Levels of nitric oxide (NO), TNF-α, and IL-10 were significantly altered post-EMP exposure.
- p38 pathway proteins (total and phosphorylated) increased significantly after EMP exposure.
- Inhibition of p38 partly prevented EMP-induced changes in cytokine and NO levels.
Conclusions:
- EMP exposure activates microglia in the rat brain and affects their secretory function.
- The p38 signaling pathway plays a role in EMP-induced microglia activation and the subsequent inflammatory response.
