PURPOSE: Microglia activation plays a pivotal role in the initiation and progression of central nervous system (CNS) insult. The aim of the present work was to investigate the activation of microglia and involvement of signal transducer and activator of transcription 3 (STAT3) in microglia activation after 2.45 GHz electromagnetic fields (EMF) exposure. MATERIALS AND METHODS: In this study, murine N9 microglial cells were exposed to 2.45 GHz EMF, the protein expressions of STAT3, Janus Tyrosine kinase 1 and 2(JAK1 and JAK2), phosphor-(Try705)STAT3 and DNA binding activity of STAT3 were examined by Western blot analysis and electrophoresis mobility shift assay (EMSA). Levels of the nitric oxide (NO) derivative nitrite were determined in the culture medium by the Griess reaction. The mRNA expression of tumour necrosis factor alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS) were detected by reverse transcription and polymerase chain reaction (RT-PCR). RESULTS: A significant increase of STAT3 DNA-binding ability was noted after exposure. Consistent with this, EMF rapidly induced phosphorylation of STAT3 and activated JAK1 and JAK2. In addition, EMF exposure increased transcription levels of the inflammation-associated genes, iNOS and TNF-alpha, which are reported to contain STAT-binding elements in their promoter region. P6, a JAK inhibitor, reduced induction of iNOS and TNF-alpha, nuclear factor binding activity, and activation of STAT3 in EMF-stimulated microglia. CONCLUSION: These results provide evidence that EMF exposure can initiate the activation of microglia cells and STAT3 signalling involves in EMF-induced microglial activation.
PURPOSE: Microglia activation plays a pivotal role in the initiation and progression of central nervous system (CNS) insult. The aim of the present work was to investigate the activation of microglia and involvement of signal transducer and activator of transcription 3 (STAT3) in microglia activation after 2.45 GHz electromagnetic fields (EMF) exposure. MATERIALS AND METHODS: In this study, murine N9 microglial cells were exposed to 2.45 GHz EMF, the protein expressions of STAT3, Janus Tyrosine kinase 1 and 2(JAK1 and JAK2), phosphor-(Try705)STAT3 and DNA binding activity of STAT3 were examined by Western blot analysis and electrophoresis mobility shift assay (EMSA). Levels of the nitric oxide (NO) derivative nitrite were determined in the culture medium by the Griess reaction. The mRNA expression of tumour necrosis factor alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS) were detected by reverse transcription and polymerase chain reaction (RT-PCR). RESULTS: A significant increase of STAT3 DNA-binding ability was noted after exposure. Consistent with this, EMF rapidly induced phosphorylation of STAT3 and activated JAK1 and JAK2. In addition, EMF exposure increased transcription levels of the inflammation-associated genes, iNOS and TNF-alpha, which are reported to contain STAT-binding elements in their promoter region. P6, a JAK inhibitor, reduced induction of iNOS and TNF-alpha, nuclear factor binding activity, and activation of STAT3 in EMF-stimulated microglia. CONCLUSION: These results provide evidence that EMF exposure can initiate the activation of microglia cells and STAT3 signalling involves in EMF-induced microglial activation.