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Sheikh, A.Q.; Taghian, T.; Hemingway, B.; Cho, H.; Kogan, A.B.; Narmoneva, D.A. |
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Title |
Regulation of endothelial MAPK/ERK signalling and capillary morphogenesis by low-amplitude electric field |
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Journal Article |
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Year |
2013 |
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Journal of the Royal Society, Interface / the Royal Society |
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10 |
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78 |
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20120548-20120548 |
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Keywords |
Animals; Apoptosis; Calcium; Calcium: metabolism; Capillaries; Capillaries: cytology; Capillaries: growth & development; Cell Proliferation; Cells; Cultured; Electromagnetic Fields; Extracellular Signal-Regulated MAP Kinases; Extracellular Signal-Regulated MAP Kinases: metabo; Gene Expression Regulation; MAP Kinase Kinase 4; MAP Kinase Kinase 4: metabolism; MAP Kinase Signaling System; Mice; Morphogenesis; Neovascularization; Phosphatidylinositol 3-Kinases; Phosphatidylinositol 3-Kinases: metabolism; Phosphorylation; Physiologic; Proto-Oncogene Proteins c-raf; Proto-Oncogene Proteins c-raf: metabolism; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor A: biosynthesis |
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Low-amplitude electric field (EF) is an important component of wound-healing response and can promote vascular tissue repair; however, the mechanisms of action on endothelium remain unclear. We hypothesized that physiological amplitude EF regulates angiogenic response of microvascular endothelial cells via activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. A custom set-up allowed non-thermal application of EF of high (7.5 GHz) and low (60 Hz) frequency. Cell responses following up to 24 h of EF exposure, including proliferation and apoptosis, capillary morphogenesis, vascular endothelial growth factor (VEGF) expression and MAPK pathways activation were quantified. A db/db mouse model of diabetic wound healing was used for in vivo validation. High-frequency EF enhanced capillary morphogenesis, VEGF release, MEK-cRaf complex formation, MEK and ERK phosphorylation, whereas no MAPK/JNK and MAPK/p38 pathways activation was observed. The endothelial response to EF did not require VEGF binding to VEGFR2 receptor. EF-induced MEK phosphorylation was reversed in the presence of MEK and Ca(2+) inhibitors, reduced by endothelial nitric oxide synthase inhibition, and did not depend on PI3K pathway activation. The results provide evidence for a novel intracellular mechanism for EF regulation of endothelial angiogenic response via frequency-sensitive MAPK/ERK pathway activation, with important implications for EF-based therapies for vascular tissue regeneration. |
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UNIBAS @ david.schuermann @ |
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562 |
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Messiha, H.L.; Wongnate, T.; Chaiyen, P.; Jones, A.R.; Scrutton, N.S. |
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Title |
Magnetic field effects as a result of the radical pair mechanism are unlikely in redox enzymes |
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2015 |
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Journal of the Royal Society, Interface / the Royal Society |
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12 |
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20141155-20141155 |
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biochemistry; biophysics |
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Environmental exposure to electromagnetic fields is potentially carcinogenic. The radical pair mechanism is considered the most feasible mechanism of interaction between weak magnetic fields encountered in our environment and biochemical systems. Radicals are abundant in biology, both as free radicals and reaction intermediates in enzyme mechanisms. The catalytic cycles of some flavin-dependent enzymes are either known or potentially involve radical pairs. Here, we have investigated the magnetic field sensitivity of a number of flavoenzymes with important cellular roles. We also investigated the magnetic field sensitivity of a model system involving stepwise reduction of a flavin analogue by a nicotinamide analogue-a reaction known to proceed via a radical pair. Under the experimental conditions used, magnetic field sensitivity was not observed in the reaction kinetics from stopped-flow measurements in any of the systems studied. Although widely implicated in radical pair chemistry, we conclude that thermally driven, flavoenzyme-catalysed reactions are unlikely to be influenced by exposure to external magnetic fields. |
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UNIBAS @ david.schuermann @ |
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633 |
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Fedele, G.; Edwards, M.D.; Bhutani, S.; Hares, J.M.; Murbach, M.; Green, E.W.; Dissel, S.; Hastings, M.H.; Rosato, E.; Kyriacou, C.P. |
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Genetic Analysis of Circadian Responses to Low Frequency Electromagnetic Fields in <italic>Drosophila melanogaster</italic> |
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Journal Article |
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2014 |
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PLoS Genet |
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PLoS Genet |
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10 |
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12 |
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e1004804EP - |
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<title>Author Summary</title> <p>Low frequency electromagnetic fields (EMFs) are associated with electrical power lines and have been implicated in the development of childhood leukemias. However, the Earth also has a natural EMF that animals can detect and which they use in order to navigate and orient themselves, particularly during migrations. One way they might do this is by using specialised photoreceptors called cryptochromes, which when activated by light, generate changes within the molecule that are susceptible to EMFs. Cryptochromes are important components of animal circadian clocks, the 24 hour timers that determine daily behavioral and physiological cycles. We have studied the circadian behavior of the fruitfly and have observed some novel and robust effects of EMFs on the fly's sleep-wake cycle that are mediated by cryptochrome. By using cryptochrome mutants we find that our results do not support the classic model for how this molecule might respond to EMFs. We also show that mammalian cryptochromes can respond to EMF when placed into transgenic Drosophila, whereas in mammalian clock neurons, they cannot. Consequently, the EMF responsiveness of cryptochrome is determined by its intracellular environment, suggesting that other, unknown molecules that interact with cryptochrome are also very important.</p> |
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Public Library of Science |
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WP5 In vitro; WP6 In vivo |
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UNIBAS @ david.schuermann @ |
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635 |
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Vergallo, C.; Ahmadi, M.; Mobasheri, H.; Dini, L. |
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Impact of Inhomogeneous Static Magnetic Field (31.7–232.0 mT) Exposure on Human Neuroblastoma SH-SY5Y Cells during Cisplatin Administration |
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2014 |
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PLoS ONE |
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9 |
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e113530-e113530 |
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UNIBAS @ david.schuermann @ |
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627 |
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Lu, Y.; He, M.; Zhang, Y.; Xu, S.; Zhang, L.; He, Y.; Chen, C.; Liu, C.; Pi, H.; Yu, Z.; Zhou, Z. |
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Title |
Differential Pro-Inflammatory Responses of Astrocytes and Microglia Involve STAT3 Activation in Response to 1800 MHz Radiofrequency Fields |
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Journal Article |
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Year |
2014 |
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PloS one |
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9 |
Issue |
9 |
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e108318-e108318 |
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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-1β, TNF-α, 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. |
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UNIBAS @ david.schuermann @ |
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555 |
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