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Fifty-Hertz Magnetic Field Affects the Epigenetic Modulation of the miR-34b/c in Neuronal Cells

TitleFifty-Hertz Magnetic Field Affects the Epigenetic Modulation of the miR-34b/c in Neuronal Cells
Publication TypeArticolo su Rivista peer-reviewed
Year of Publication2017
AuthorsConsales, Claudia, Cirotti C., Filomeni G., Panatta M., Butera A., Merla Caterina, Lopresto Vanni, Pinto Rosanna, Marino Carmela, and Benassi Barbara
JournalMolecular Neurobiology
Volume55
Pagination1-17
ISSN08937648
Keywordsacetylcysteine, alpha synuclein, alpha-Synuclein, animal, animal cell, Animals, article, Base Sequence, Biological, biological model, brain cell, brain cortex, C57BL mouse, Cell Line, Cerebral Cortex, computer model, controlled study, CpG island, cytology, DNA Methylation, Epigenesis, epigenetics, gene control, Gene expression, gene targeting, Genetic, genetic epigenesis, genetic transcription, genetics, glutathione ethyl ester, human, human cell, Humans, in vitro study, Inbred C57BL, magnetic field, Magnetic fields, metabolism, Mice, microRNA, microRNA 34b, microRNA 34c, MicroRNAs, MIRN34 microRNA, Mitochondria, mitochondrion, Models, mouse, nerve cell, Neurons, nonhuman, nucleotide sequence, oxidation reduction reaction, Oxidation-Reduction, Oxidative stress, Phenotype, promoter region, Promoter Regions, protein p53, reactive oxygen metabolite, SH-SY5Y cell line, Transcription, Tumor, tumor cell line, Tumor Suppressor Protein p53, unclassified drug
Abstract

The exposure to extremely low-frequency magnetic fields (ELF-MFs) has been associated to increased risk of neurodegenerative diseases, although the underlying molecular mechanisms are still undefined. Since epigenetic modulation has been recently encountered among the key events leading to neuronal degeneration, we here aimed at assessing if the control of gene expression mediated by miRNAs, namely miRs-34, has any roles in driving neuronal cell response to 50-Hz (1 mT) magnetic field in vitro. We demonstrate that ELF-MFs drive an early reduction of the expression level of miR-34b and miR-34c in SH-SY5Y human neuroblastoma cells, as well as in mouse primary cortical neurons, by affecting the transcription of the common pri-miR-34. This modulation is not p53 dependent, but attributable to the hyper-methylation of the CpG island mapping within the miR-34b/c promoter. Incubation with N-acetyl-l-cysteine or glutathione ethyl-ester fails to restore miR-34b/c expression, suggesting that miRs-34 are not responsive to ELF-MF-induced oxidative stress. By contrast, we show that miRs-34 control reactive oxygen species production and affect mitochondrial oxidative stress triggered by ELF-MFs, likely by modulating mitochondria-related miR-34 targets identified by in silico analysis. We finally demonstrate that ELF-MFs alter the expression of the α-synuclein, which is specifically stimulated upon ELF-MFs exposure via both direct miR-34 targeting and oxidative stress. Altogether, our data highlight the potential of the ELF-MFs to tune redox homeostasis and epigenetic control of gene expression in vitro and shed light on the possible mechanism(s) producing detrimental effects and predisposing neurons to degeneration. © 2017 Springer Science+Business Media, LLC

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URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85031930225&doi=10.1007%2fs12035-017-0791-0&partnerID=40&md5=5c46871e937da54c35201959ccd7bee7
DOI10.1007/s12035-017-0791-0
Citation KeyConsales20171