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      Exposure to Extremely Low-Frequency Electromagnetic Fields Modulates Na + Currents in Rat Cerebellar Granule Cells through Increase of AA/PGE 2 and EP Receptor-Mediated cAMP/PKA Pathway

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          Abstract

          Although the modulation of Ca 2+ channel activity by extremely low-frequency electromagnetic fields (ELF-EMF) has been studied previously, few reports have addressed the effects of such fields on the activity of voltage-activated Na + channels (Na v). Here, we investigated the effects of ELF-EMF on Na v activity in rat cerebellar granule cells (GCs). Our results reveal that exposing cerebellar GCs to ELF-EMF for 10–60 min significantly increased Na v currents ( I Na) by 30–125% in a time- and intensity-dependent manner. The Na v channel steady-state activation curve, but not the steady-state inactivation curve, was significantly shifted (by 5.2 mV) towards hyperpolarization by ELF-EMF stimulation. This phenomenon is similar to the effect of intracellular application of arachidonic acid (AA) and prostaglandin E 2 (PGE 2) on I Na in cerebellar GCs. Increases in intracellular AA, PGE 2 and phosphorylated PKA levels in cerebellar GCs were observed following ELF-EMF exposure. Western blottings indicated that the Na V 1.2 protein on the cerebellar GCs membrane was increased, the total expression levels of Na V 1.2 protein were not affected after exposure to ELF-EMF. Cyclooxygenase inhibitors and PGE 2 receptor (EP) antagonists were able to eliminate this ELF-EMF-induced increase in phosphorylated PKA and I Na. In addition, ELF-EMF exposure significantly enhanced the activity of PLA 2 in cerebellar GCs but did not affect COX-1 or COX-2 activity. Together, these data demonstrate for the first time that neuronal I Na is significantly increased by ELF-EMF exposure via a cPLA2 AA PGE 2 EP receptors PKA signaling pathway.

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          Prostanoid receptors: structures, properties, and functions.

          Shuh Narumiya, Yukihiko Sugimoto, Fumitaka Ushikubi (1999)
          Prostanoids are the cyclooxygenase metabolites of arachidonic acid and include prostaglandin (PG) D(2), PGE(2), PGF(2alpha), PGI(2), and thromboxne A(2). They are synthesized and released upon cell stimulation and act on cells in the vicinity of their synthesis to exert their actions. Receptors mediating the actions of prostanoids were recently identified and cloned. They are G protein-coupled receptors with seven transmembrane domains. There are eight types and subtypes of prostanoid receptors that are encoded by different genes but as a whole constitute a subfamily in the superfamily of the rhodopsin-type receptors. Each of the receptors was expressed in cultured cells, and its ligand-binding properties and signal transduction pathways were characterized. Moreover, domains and amino acid residues conferring the specificities of ligand binding and signal transduction are being clarified. Information also is accumulating as to the distribution of these receptors in the body. It is also becoming clear for some types of receptors how expression of their genes is regulated. Furthermore, the gene for each of the eight types of prostanoid receptor has been disrupted, and mice deficient in each type of receptor are being examined to identify and assess the roles played by each receptor under various physiological and pathophysiological conditions. In this article, we summarize these findings and attempt to give an overview of the current status of research on the prostanoid receptors.
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            Voltage-gated sodium channel expression and potentiation of human breast cancer metastasis.

            Carlo Palmieri, J Slade, Esra Battaloglu … (2005)
            Ion channel activity is involved in several basic cellular behaviors that are integral to metastasis (e.g., proliferation, motility, secretion, and invasion), although their contribution to cancer progression has largely been ignored. The purpose of this study was to investigate voltage-gated Na(+) channel (VGSC) expression and its possible role in human breast cancer. Functional VGSC expression was investigated in human breast cancer cell lines by patch clamp recording. The contribution of VGSC activity to directional motility, endocytosis, and invasion was evaluated by in vitro assays. Subsequent identification of the VGSC alpha-subunit(s) expressed in vitro was achieved using reverse transcription-PCR, immunocytochemistry, and Western blot techniques and used to investigate VGSCalpha expression and its association with metastasis in vivo. VGSC expression was significantly up-regulated in metastatic human breast cancer cells and tissues, and VGSC activity potentiated cellular directional motility, endocytosis, and invasion. Reverse transcription-PCR revealed that Na(v)1.5, in its newly identified "neonatal" splice form, was specifically associated with strong metastatic potential in vitro and breast cancer progression in vivo. An antibody specific for this form confirmed up-regulation of neonatal Na(v)1.5 protein in breast cancer cells and tissues. Furthermore, a strong correlation was found between neonatal Na(v)1.5 expression and clinically assessed lymph node metastasis. Up-regulation of neonatal Na(v)1.5 occurs as an integral part of the metastatic process in human breast cancer and could serve both as a novel marker of the metastatic phenotype and a therapeutic target.
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              Epoxygenase pathways of arachidonic acid metabolism.

              D Zeldin (2001)
              Article 0 comments Cited 126 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                William Phillips: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2013
                Publication date (Electronic): 22 January 2013
                Volume: 8
                Issue: 1
                Electronic Location Identifier: e54376
                Affiliations
                [1]Institutes of Brain Science, School of Life Sciences and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, China
                University of Sydney, Australia
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: YAM YLH. Performed the experiments: YLH DDL YJF XQZ. Analyzed the data: YLH DDL JJY. Contributed reagents/materials/analysis tools: YJF XQZ JJY. Wrote the paper: YAM YLH.

                Article
                Publisher ID: PONE-D-12-24487
                DOI: 10.1371/journal.pone.0054376
                PMC ID: 3551899
                PubMed ID: 23349866
                SO-VID: ae00ef74-93e8-41c0-b11e-bc2e81e72c64
                Copyright statement: Copyright @ 2013
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 12 August 2012
                Date accepted : 11 December 2012
                Page count
                Pages: 13
                Funding
                This work was supported by a grant from the National Basic Research Program of China (2011CB503703) and the Shanghai Leading Academic Discipline Project [B111]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Model Organisms
                Subject: Animal Models
                Subject: Rat
                Subject: Molecular Cell Biology
                Subject: Signal Transduction
                Subject: Signaling Cascades
                Subject: PKA signaling cascade
                Subject: Neuroscience
                Subject: Cellular Neuroscience
                Subject: Ion Channels
                Subject: Molecular Neuroscience
                Subject: Signaling Pathways
                Subject: Neurophysiology
                Subject: Central Nervous System
                Subject: Physics
                Subject: Electromagnetic Radiation

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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