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Original Paper

The Proliferative Response of NB69 Human Neuroblastoma Cells to a 50 Hz Magnetic Field is mediated by ERK1/2 Signaling

Martínez M.A.1 · Úbeda A.1 · Cid M.A.2 · Trillo M.A.1

Author affiliations

1Servicio de Investigación-BEM, Hospital Ramón y Cajal - IRYCIS, Madrid,2Departamento de Ciencias Biomédicas, UEM, Madrid

Corresponding Author

María Antonia, Martínez, Serv. Investigación-BEM, Hospital Ramón y Cajal - IRYCIS, Ctra. Colmenar Viejo km 9.100 ,28034 Madrid (SPAIN), Tel. +34 91 729 3475, Fax +34 91 336 8171, E-Mail m.antonia.martinez@hrc.es

Related Articles for ""

Cell Physiol Biochem 2012;29:675-686

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Abstract

A number of studies have reported that extremely low frequency magnetic fields (ELF-MF) can modulate proliferative processes in vitro; however, the transduction mechanisms implicated in such phenomena remain to be identified. The present study was aimed to determine whether a 50 Hz, 100 µT MF can induce cell proliferation in the human neuroblastoma line NB69, and whether the signaling pathway MAPK-ERK1/2 (Mitogen-Activated Protein Kinase - Extracellular-Signal-Regulated Kinase 1 and 2) is involved in that proliferative response. The cultures were exposed intermittently or continuously to the MF for a 63-hour duration. The continuous treatment did not induce significant changes in cell proliferation. In contrast, intermittent exposure caused statistically significant increase in the percent of cells in phase S of the cell cycle, followed by a significant increase in cell number. The intermittent treatment also induced an early, transient and repetitive activation of ERK1/2 that could be involved in the proliferative effects. In fact, both the proliferative response and the repeated activation of ERK1/2 were blocked by PD98059, the specific inhibitor of MEK (ERK kinases 1 and 2). Taken together, the described results indicate that a 50 Hz, 100 µT MF can stimulate proliferation in NB69 cells by triggering MAPK-ERK1/ 2 signaling at each of the “On” periods of an intermittent exposure.

© 2012 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: March 02, 2012
Published online: May 11, 2012
Issue release date: June 2012

Number of Print Pages: 12
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

For additional information: https://www.karger.com/CPB


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