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To investigate the radiofrequency field-induced proinflammatory responses of microglia and astrocytes and the involved molecular mechanisms.
STAT3 (signal transducer and activator of transcription 3) mediates signal transduction from the extracellular environment to the nucleus. To test the potential involvement of STAT3 in the response to radiofrequency fields, the STAT3 inhibitor "Stattic" was partially added to the culture medium 24 hours before the radiofrequency field exposure.
Positive controls were performed via treatment with lipopolysaccharides (1 µg/ml).
|ばく露時間||intermittent for 1, 3, 6, 12, or 24 hours (5 min on and 10 min off)|
|Repetition frequency||217 Hz|
|チャンバの詳細||cells were cultured in 35 mm plastic Petri dishes|
|ばく露装置の詳細||system consisted of two resonating waveguides; in each waveguide chamber, a Petri dish holder for six dishes ensured that each dish was positioned accurately in the H-field maximum of the standing wave; two ventilation holes were located on the waveguide, a ventilator fan was fixed to one hole to cool the culture medium; waveguides were placed in an incubator to ensure constant environmental conditions (37 ± 0.2°C, 5% CO2, 95% air atmosphere)|
|Sham exposure||A sham exposure was conducted.|
|Additional information||temperature rise due to radiofrequency field was less than 0.05°C|
Radiofrequency exposure induced activation of both cell types: After 12 and 24 hours exposure, the protein expression of CD11b in microglia was significantly increased compared to the corresponding sham exposure. In astrocytes, the protein expression of glial fibrillary acidic protein was significantly increased after 24 hours exposure compared to the sham exposure as shown via immunohistochemistry and Western blot.
Microglia and astrocytes exposed to radiofrequency fields showed both proinflammatory responses compared to the sham exposure: However, the expression and release profiles of interleukin-1alpha, tumor necrosis factor-alpha, interleukin-6, prostaglandin E2, nitric oxide, inducible nitric oxide synthase, and cyclooxygenase-2 differed between the two cell types. The expression of STAT 3 was only activated in microglia. Hence, an addition of the STAT3 inhibitor "Stattic" attenuated the exposure induced effects in microglia but not in astrocytes.
The authors conclude that exposure to radiofrequency fields induces differential proinflammatory responses in microglia and astrocytes which could be mediated through different activation of STAT3 in each cell type.