Study type: Medical/biological study (experimental study)

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

Published in: J Neuroinflammation 2010; 7: 1-13

Aim of study (acc. to author)

To study, in more detail than in a previous study (Hao et al. 2010), the activation of microglia and involvement of signal transducer and activator of transcription 3 (STAT3; mediates signal transduction from the extracellular environment to the nucleus) in microglia activation after 2.45 GHz electromagnetic fields exposure.

Background/further details

Microglia is considered as a specialised macrophages residing form in the central nervous system. In response to a variety of insults, microglia adopts an activated phenotype. Microglia activation plays a pivotal role in the initiation and progression of several neurodegenerative diseases.
Some cell samples were pretreated with the JAK inhibitor pyridone 6 (P6) to study whether P6 could affect the STAT3 activation (to further demonstrate JAK2-STAT3 signal transduction (JAK is a STAT3 activator and is able to phosphorylate STAT3)). Cells were investigated 1 h, 3 h, 6 h, 12 h, and 24 h after exposure.



Exposure Parameters
Exposure 1: 2.45 GHz
Modulation type: pulsed
Exposure duration: continuous for 20 min
  • power: 90 mW average over time
  • SAR: 6 W/kg average over time

General information

A part of the cells were pretreated with Pyridone 6

Exposure 1

Main characteristics
Frequency 2.45 GHz
Exposure duration continuous for 20 min
Modulation type pulsed
Pulse width 2 µs
Packets per second 500
Exposure setup
Exposure source
Distance between exposed object and exposure source 90 cm
Chamber anechoic chamber with a temperature of 25° C - 26° C
Setup four flasks placed in a 24.5 cm x 21 cm water bath at 37° C; irradiation directed downward from the rectangular horn antenna to the flasks by a refector
Sham exposure A sham exposure was conducted.
Measurand Value Type Method Mass Remarks
power 90 mW average over time - - -
SAR 6 W/kg average over time calculated - -

Exposed system:

Methods Endpoint/measurement parameters/methodology

Investigated system:
Time of investigation:
  • after exposure

Main outcome of study (acc. to author)

The data showed that the electromagnetic field exposure significantly induced the phosphorylation of JAK2 and STAT3 (time-dependent manner with peak at 12 h), and the DNA-binding ability of STAT3 in N9 microglia. Additionally, electromagnetic field exposure dramatically increased the expression of CD11b, tumor necrosis factor-alpha and inducible nitric oxide synthase (iNOS), and the production of nitric oxide.
P6 strongly suppressed the phosphorylation of JAK2 and STAT3 and decreased the STAT3 activity in electromagnetic field-stimulated microglia. Interestingly, expression of CD11b as well as gene expression and production of tumor necrosis factor-alpha and inducible nitric oxide synthase (iNOS) were suppressed by P6 at 12 h, but not at 3 h after electromagnetic field exposure.
In conclusion, the electromagnetic field exposure directly triggered an initial activation of microglia and produced a significant pro-inflammatory response. Activation of JAK2-STAT3 signaling occured in parallel with the microglial activation and the release of pro-inflammatory factors (i.e. tumor necrosis factor-alpha, iNOS and nitric oxide). Microglia activation and pro-inflammatory responses were significantly reduced by P6 at 12 h, but not at 3 h after electromagnetic field exposure. These data suggest that the JAK2-STAT3 pathway may not mediate the initial microglial activation but does promote pro-inflammatory responses in electromagnetic field-stimulated microglial cells. The data provide a basis to determine whether the pro-inflammatory responses of electromagnetic field-stimulated microglia can be suppressed by inhibition of the JAK2-STAT3 pathway in therapeutic interventions.

Study character:

Study funded by

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