6,486 Studies Reviewed. 85.2% of Original Studies Found Biological Effects. The Evidence is Clear.
Shield Your Body
Brain & Nervous System

The role of the JAK2-STAT3 pathway in pro-inflammatory responses of EMF-stimulated N9 microglial cells

Bioeffects Seen

Yang X, He G, Hao Y, Chen C, Li M, Wang Y, Zhang G, Yu Z · 2010

View Original Abstract
Share:

EMF stimulation of N9 microglia triggered pro-inflammatory responses, and the JAK2-STAT3 pathway promoted those responses but may not have mediated the initial microglial activation.

Plain English Summary

Summary written for general audiences

Researchers studied how electromagnetic field exposure affects N9 microglial cells and the role of the JAK2-STAT3 signaling pathway in any resulting pro-inflammatory responses. EMF significantly induced phosphorylation of JAK2 and STAT3, and also dramatically increased the expression of CD11b, TNF-α, and iNOS, and the production of NO. When cells were pretreated with the JAK inhibitor P6, phosphorylation of JAK2 and STAT3 was strongly suppressed, and expression of CD11b, TNF-α, and iNOS was suppressed at 12 hours but not at 3 hours after EMF exposure.

Why This Matters

The researchers used N9 microglial cells treated with EMF or a sham treatment, with or without pretreatment with P6, an inhibitor of the Janus family of tyrosine kinases. Microglial activation was assessed using the marker CD11b, while iNOS, TNF-α, and NO levels were measured using RT-PCR, ELISA, and the nitrate reductase method. P6 suppressed expression of CD11b, TNF-α, and iNOS at 12 hours but not at 3 hours after EMF exposure, while the JAK2-STAT3 pathway may not mediate the initial microglial activation but does promote pro-inflammatory responses. The researchers suggested that the JAK2-STAT3 pathway might be a therapeutic target for reducing pro-inflammatory responses in EMF-activated microglia.

Exposure Details

SAR
6 W/kg
Source/Device
2.45 GHz
Exposure Duration
20-min

Exposure Context

This study used 6 W/kg for SAR (device absorption):

Building Biology guidelines are practitioner-based limits from real-world assessments. BioInitiative Report recommendations are based on peer-reviewed science. Check Your Exposure to compare your own measurements.

Where This Falls on the Concern Scale

Study Exposure Level in ContextStudy Exposure Level in ContextThis study: 6 W/kgExtreme Concern - 0.1 W/kgFCC Limit - 1.6 W/kgEffects observed in the Extreme Concern range (Building Biology)This level is 4 times the FCC limit
A logarithmic frequency spectrum from 10 Hz to 100 GHz showing where this study's 2.45 GHz exposure sits relative to common EMF sources.Where This Frequency Sits on the EMF SpectrumELFVLFLF / MFHF / VHFUHFSHFmm10 Hz100 GHzThis study: 2.45 GHzPower lines50/60 Hz5G mm28 GHzLogarithmic scale

Study Details

we investigated the role of STAT3 signaling in EMF-induced microglial activation and pro-inflammatory responses in more detail than the previous study.

N9 microglial cells were treated with EMF exposure or a sham treatment, with or without pretreatment...

EMF was found to significantly induce phosphorylation of JAK2 and STAT3, and DNA-binding ability of ...

EMF exposure directly triggers initial activation of microglia and produces a significant pro-inflammatory response. Our findings confirm that the JAK2-STAT3 pathway may not mediate this initial microglial activation but does promote pro-inflammatory responses in EMF-stimulated microglial cells. Thus, the JAK2-STAT3 pathway might be a therapeutic target for reducing pro-inflammatory responses in EMF-activated microglia.

Cite This Study
Yang X, He G, Hao Y, Chen C, Li M, Wang Y, Zhang G, Yu Z (2010). The role of the JAK2-STAT3 pathway in pro-inflammatory responses of EMF-stimulated N9 microglial cells J Neuroinflammation. 7:54, 2010.
Show BibTeX
@article{x_2010_the_role_of_the_208,
  author = {Yang X and He G and Hao Y and Chen C and Li M and Wang Y and Zhang G and Yu Z},
  title = {The role of the JAK2-STAT3 pathway in pro-inflammatory responses of EMF-stimulated N9 microglial cells},
  year = {2010},
  doi = {10.1186/1742-2094-7-54},
  url = {https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-7-54},
}
DOI: 10.1186/1742-2094-7-54

Cited By (95 papers)

View all 95 citing papers on Semantic Scholar

Quick Questions About This Study

The study used N9 microglial cells treated with EMF or a sham treatment.
EMF dramatically increased the expression of CD11b, TNF-α, and iNOS, and the production of NO.
P6 strongly suppressed the phosphorylation of JAK2 and STAT3 and diminished STAT3 activity, and it suppressed expression of CD11b, TNF-α, and iNOS at 12 hours but not at 3 hours after EMF exposure.
The findings suggest the JAK2-STAT3 pathway may not mediate the initial microglial activation but does promote pro-inflammatory responses in EMF-stimulated microglial cells.
Activation of JAKs and STAT3 proteins was evaluated by western blotting for specific tyrosine phosphorylation, and STAT3's ability to bind to DNA was detected with an electrophoresis mobility shift assay.