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Updated: Jun 17, 2025
3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
Published on: June 2, 2014
Study on the involvement of microglial S100A8 in neuroinflammation and microglia activation during migraine attacks
Ning An1, Yingying Zhang2, Jinding Xie3
1Department of Neurology, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China; Department of Neurology, Affiliated Hongqi Hospital of Mudanjiang Medical University, Mudanjiang, Heilongjiang, China.
Background:
Microglia is the primary source of inflammatory factors during migraine attacks. This study aims to investigate the role of microglia related genes (MRGs) in migraine attacks.
Methods:
The RNA sequencing results of migraineurs and the panglaodb database were used to obtain differentially expressed genes (DEGs) in migraine related to microglia. A migraine rat model was established for validating and localizing of the MRGs, and subsequent screening for target genes was conducted. A shRNA was designed to interference the expression of target genes and administered into the trigeminal ganglion (TG) of rats. Pain sensitivity in rats was evaluated via the hot water tail-flick (HWTF) and formalin-induced pain (FIP) experiments. ELISA was used to quantify the levels of inflammatory cytokines and CGRP. WB and immunofluorescence assays were applied to detect the activation of microglia.
Results:
A total of five DEGs in migraine related to microglia were obtained from RNA sequencing and panglaodb database. Animal experiments showed that these genes expression were heightened in the TG and medulla oblongata (MO) of migraine rats. The gene S100A8 co-localized with microglia in both TG and MO. The HWTF and FIP experiments demonstrated that interference with S100A8 alleviated the sense of pain in migraine rats. Moreover, the levels of TNFα, IL-1β, IL-6, and CGRP in the TG and MO of rats in the model rats were increased, and the expression of microglia markers IBA-1, M1 polarization markers CD86 and iNOS was upregulated. Significantly, interference with S100A8 reversed these indicators.
Conclusion:
Interference with S100A8 in microglia increased the pain threshold during migraine attacks, and inhibited neuroinflammation and microglia activation.
Insights
Targeting S100A8 in microglia reduces pain and neuroinflammation during migraine attacks. This study highlights S100A8 as a potential therapeutic target for migraine relief.
Area of Science:
- Neuroscience
- Immunology
Background:
- Microglia are key inflammatory mediators in migraine.
- Investigating microglia-related genes (MRGs) is crucial for understanding migraine pathogenesis.
Purpose of the Study:
- To identify and characterize MRGs involved in migraine.
- To explore the therapeutic potential of targeting specific MRGs in migraine.
Main Methods:
- Differential gene expression analysis using RNA sequencing and the panglaodb database.
- Establishment of a migraine rat model to validate MRGs in the trigeminal ganglion (TG) and medulla oblongata (MO).
- RNA interference (shRNA) targeting S100A8 in the TG, followed by pain sensitivity tests (HWTF, FIP), ELISA for cytokines and CGRP, and Western blot/immunofluorescence for microglia activation markers.
Main Results:
- Five MRGs were identified; S100A8 expression was elevated in the TG and MO of migraine rats and co-localized with microglia.
- Interference with S100A8 significantly alleviated pain sensitivity in the migraine rat model.
- S100A8 inhibition reversed the upregulation of pro-inflammatory cytokines (TNFα, IL-1β, IL-6, CGRP) and microglia activation markers (IBA-1, CD86, iNOS).
Conclusions:
- Targeting S100A8 in microglia enhances pain threshold during migraine attacks.
- Inhibition of S100A8 effectively suppresses neuroinflammation and microglia activation in migraine.
