ID Number		2479
Study Type		In Vitro
Model		In vitro studies of neural cells exposed to RF and 50 Hz: 1) Embryonic neural stem cells (eNSCs) exposed to 1800 MHz at 1, 2, and 4 W/kg for 1, 2, and 3 days were examined for apoptosis, proliferation, cell cycle or the mRNA expressions of related genes, ratio of NSC differentiated neurons and astrocytes, neurite outgrowth, and mRNA and protein expression of the proneural genes Ngn1 and NeuroD, 2) pro-inflammatory responses of astrocytes and microglia exposed to 1800 MHz.
Details		AUTHORS' ABSTRACT: Chen et al. 2014 (IEEE #5980): A radiofrequency electromagnetic field (RF-EMF) of 1800 MHz is widely used in mobile communications. However, the effects of RF-EMFs on cell biology are unclear. Embryonic neural stem cells (eNSCs) play a critical role in brain development. Thus, detecting the effects of RF-EMF on eNSCs is important for exploring the effects of RF-EMF on brain development. Here, we exposed eNSCs to 1800MHz RF-EMF at specific absorption rate (SAR) values of 1, 2, and 4W/kg for 1, 2, and 3 days. We found that 1800MHz RF-EMF exposure did not influence eNSC apoptosis, proliferation, cell cycle or the mRNA expressions of related genes. RF-EMF exposure also did not alter the ratio of eNSC differentiated neurons and astrocytes. However, neurite outgrowth of eNSC differentiated neurons was inhibited after 4W/kg RF-EMF exposure for 3 days. Additionally, the mRNA and protein expression of the proneural genes Ngn1 and NeuroD, which are crucial for neurite outgrowth, were decreased after RF-EMF exposure. The expression of their inhibitor Hes1 was upregulated by RF-EMF exposure. These results together suggested that 1800MHz RF-EMF exposure impairs neurite outgrowth of eNSCs. More attention should be given to the potential adverse effects of RF-EMF exposure on brain development. AUTHORS' ABSTRACT: Lu et al. 2014 (IEEE #5997): Microglia and astrocytes play important role in maintaining the homeostasis of central nervous system (CNS). Several CNS impacts have been postulated to be associated with radiofrequency (RF) electromagnetic fields exposure. Given the important role of inflammation in neural physiopathologic processes, we investigated the pro-inflammatory responses of microglia and astrocytes and the involved mechanism in response to RF fields. Microglial N9 and astroglial C8-D1A cells were exposed to 1800 MHz RF for different time with or without pretreatment with STAT3 inhibitor. Microglia and astrocytes were activated by RF exposure indicated by up-regulated CD11b and glial fibrillary acidic protein (GFAP). However, RF exposure induced differential pro-inflammatory responses in astrocytes and microglia, characterized by different expression and release profiles of IL-1², TNF-±, IL-6, PGE2, nitric oxide (NO), inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). Moreover, the RF exposure activated STAT3 in microglia but not in astrocytes. Furthermore, the STAT3 inhibitor Stattic ameliorated the RF-induced release of pro-inflammatory cytokines in microglia but not in astrocytes. Our results demonstrated that RF exposure differentially induced pro-inflammatory responses in microglia and astrocytes, which involved differential activation of STAT3 in microglia and astrocytes. Our data provide novel insights into the potential mechanisms of the reported CNS impacts associated with mobile phone use and present STAT3 as a promising target to protect humans against increasing RF exposure. AUTHORS' ABSTRACT: He et al. 2016 (IEEE #6556): Background: Prostaglandin E2 (PGE2)-involved neuroinflammatory processes are prevalent in several neurological conditions and diseases. Amyloid burden is correlated with the activation of E-prostanoid (EP) 2 receptors by PGE2 in Alzheimers disease. We previously demonstrated that electromagnetic field (EMF) exposure can induce pro-inflammatory responses and the depression of phagocytosis in microglial cells, but the signaling pathways involved in phagocytosis of fibrillar ²-amyloid (fA²) in microglial cells exposed to EMF are poorly understood. Given the important role of PGE2 in neural physiopathological processes, we investigated the PGE2-related signaling mechanism in the immunomodulatory phagocytosis of EMF-stimulated N9 microglial cells (N9 cells). Methods: N9 cells were exposed to EMF with or without pretreatment with the selective inhibitors of cyclooxygenase-2 (COX-2), Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), and mitogen-activated protein kinases (MAPKs) and antagonists of PG receptors EP1-4. The production of endogenous PGE2 was quantified by enzyme immunoassays. The phagocytic ability of N9 cells was evaluated based on the fluorescence intensity of the engulfed fluorescent-labeled fibrillar ²-amyloid peptide (1-42) (fA²42) measured using a flow cytometer and a fluorescence microscope. The effects of pharmacological agents on EMF-activated microglia were investigated based on the expressions of JAK2, STAT3, p38/ERK/JNK MAPKs, COX-2, microsomal prostaglandin E synthase-1 (mPGES-1), and EP2 using real-time PCR and/or western blotting. Results: EMF exposure significantly increased the production of PGE2 and decreased the phagocytosis of fluorescent-labeled fA²42 by N9 cells. The selective inhibitors of COX-2, JAK2, STAT3, and MAPKs clearly depressed PGE2 release and ameliorated microglial phagocytosis after EMF exposure. Pharmacological agents suppressed the phosphorylation of JAK2-STAT3 and MAPKs, leading to the amelioration of the phagocytic ability of EMF-stimulated N9 cells. Antagonist studies of EP1-4 receptors showed that EMF depressed the phagocytosis of fA²42 through the PGE2 system, which is linked to EP2 receptors.
Findings		Effects
Status		Completed With Publication
Principal Investigator		Third Military Med Univ, Chongqing, China
Funding Agency		?????
Country		CHINA
References		Chen, C et al. Sci Rep. , (2014) 4:-(10 pages) Lu, Y et al. PLoS One., (2014) 9:- He, GL et al. Journal of Neuroinflammation., (2016) 13:296- Wang, X et al. Cell Physiol Biochem., (2015) 37:1075-1088 Ma, Q et al. PLoS One. 2016 Mar 7;11(3):., (2016) 11:e0150923- Chen, C et al. Front. Cell Dev. Biol., (2021) doi.org/10.3389/fcell.2021.657623:- Li, Y et al. Front. Public Health. , (2021) 9:771508-(13 pages)
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