ArticleJournal of neuroinflammation2010
The role of the JAK2-STAT3 pathway in pro-inflammatory responses of EMF-stimulated N9 microglial cells.
Article in Journal of neuroinflammation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Molecular mechanisms of microglia- and astrocyte-driven neurorestoration triggered by application of electromagnetic fields.Croatian medical journal · 2019Pooled it
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- Electromagnetic Field Stimulation Effects on Intrinsically Disordered Proteins and Their Role in Aging and Neurodegeneration.Journal of biomedical science and engineering · 2025Article
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- MicroRNA-204-5p Deficiency within the vmPFC Region Contributes to Neuroinflammation and Behavioral Disorders via the JAK2/STAT3 Signaling Pathway in Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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- Chemical Constituents from the Fruit ofAntioxidants (Basel, Switzerland) · 2024Article
- Effect of Electromagnetic Field on Proliferation and Migration of Fibroblasts and Keratinocytes: Implications in Wound Healing and Regeneration.Journal of biotechnology and biomedicine · 2024Article
- Electromagnetic Field Stimulation Therapy for Alzheimer's Disease.Neurology (Chicago, Ill.) · 2024Article
- Exposure to Low Levels of Radiofrequency Electromagnetic Fields Emitted from Cell-phones as a Promising Treatment of Alzheimer's Disease: A Scoping Review Study.Journal of biomedical physics & engineering · 2023Article
- Transcranial Electromagnetic Treatment "Rebalances" Blood and Brain Cytokine Levels in Alzheimer's Patients: A New Mechanism for Reversal of Their Cognitive Impairment.Frontiers in aging neuroscience · 2022Article
- Neuropathophysiology of coronavirus disease 2019: neuroinflammation and blood brain barrier disruption are critical pathophysiological processes that contribute to the clinical symptoms of SARS-CoV-2 infection.Inflammopharmacology · 2021Review
- Inhibition of Retinal Ganglion Cell Loss By a Novel ROCK Inhibitor (E212) in Ischemic Optic Nerve Injury Via Antioxidative and Anti-Inflammatory Actions.Investigative ophthalmology & visual science · 2021Article
- Venlafaxine Attenuated the Cognitive and Memory Deficit in Mice Exposed to Isoflurane Alone.Frontiers in neurology · 2021Article
- Therapeutic Targeting Strategies for Early- to Late-Staged Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Curcumin attenuates inflammation and cell apoptosis through regulating NF-κB and JAK2/STAT3 signaling pathway against acute kidney injury.Cell cycle (Georgetown, Tex.) · 2020Article
- Effect of mobile phone radiation on oxidative stress, inflammatory response, and contextual fear memory in Wistar rat.Environmental science and pollution research international · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn several neuropathological conditions, microglia can become overactivated and cause neurotoxicity by initiating neuronal damage in response to pro-inflammatory stimuli. Our previous studies have shown that exposure to electromagnetic fields (EMF) activates cultured microglia to produce tumor necrosis factor (TNF)-α and nitric oxide (NO) through signal transduction involving the activator of transcription STAT3. Here, we investigated the role of STAT3 signaling in EMF-induced microglial activation and pro-inflammatory responses in more detail than the previous study.
methodsN9 microglial cells were treated with EMF exposure or a sham treatment, with or without pretreatment with an inhibitor (Pyridone 6, P6) of the Janus family of tyrosine kinases (JAK). The activation state of microglia was assessed via immunoreaction using the microglial marker CD11b. Levels of inducible nitric oxide synthase (iNOS), TNF-α and NO were measured using real-time reverse transcription-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and the nitrate reductase method. Activation of JAKs and STAT3 proteins was evaluated by western blotting for specific tyrosine phosphorylation. The ability of STAT3 to bind to DNA was detected with an electrophoresis mobility shift assay (EMSA).
resultsEMF was found to significantly induce phosphorylation of JAK2 and STAT3, and DNA-binding ability of STAT3 in N9 microglia. In addition, 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 in EMF-stimulated microglia. Interestingly, expression of CD11b as well as gene expression and production of TNF-α and iNOS were suppressed by P6 at 12 h, but not at 3 h, after EMF exposure.
conclusionsEMF 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.
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