Exposure of murine cells to pulsed electromagnetic fields rapidly activates the mTOR signaling pathway†
Thomas E. Patterson
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorYoshitada Sakai
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorMark D. Grabiner
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Department of Movement Sciences, University of Illinois at Chicago, Chicago, Illinois
Search for more papers by this authorMichael Ibiwoye
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorRonald J. Midura
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorMaciej Zborowski
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorCorresponding Author
Alan Wolfman
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Department of Cell Biology, NC10, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195.Search for more papers by this authorThomas E. Patterson
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorYoshitada Sakai
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorMark D. Grabiner
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Department of Movement Sciences, University of Illinois at Chicago, Chicago, Illinois
Search for more papers by this authorMichael Ibiwoye
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorRonald J. Midura
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorMaciej Zborowski
Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Search for more papers by this authorCorresponding Author
Alan Wolfman
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio
Department of Cell Biology, NC10, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195.Search for more papers by this authorConflict of Interest: The authors have no significant past or present situation that plausibly might affect the ability of any of them to make disinterested scientific judgments related to the work.
Abstract
Murine pre-osteoblasts and fibroblast cell lines were used to determine the effect of pulsed electromagnetic field (PEMF) exposure on the production of autocrine growth factors and the activation of early signal transduction pathways. Exposure of pre-osteoblast cells to PEMF minimally increased the amount of secreted TGF-β after 1 day, but had no significant effects thereafter. PEMF exposure of pre-osteoblast cells also had no effect on the amount of prostaglandin E2 in the conditioned medium. Exposure of both pre-osteoblasts and fibroblasts to PEMF rapidly activated the mTOR signaling pathway, as evidenced by increased phosphorylation of mTOR, p70 S6 kinase, and the ribosomal protein S6. Inhibition of PI3-kinase activity with the chemical inhibitor LY294002 blocked PEMF-dependent activation of mTOR in both the pre-osteoblast and fibroblast cell lines. These findings suggest that PEMF exposure might function in a manner analogous to soluble growth factors by activating a unique set of signaling pathways, inclusive of the PI-3 kinase/mTOR pathway. Bioelectromagnetics 27:535–544, 2006. © 2006 Wiley-Liss, Inc.
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