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Weak power frequency magnetic fields induce microtubule cytoskeleton reorganization depending on the epidermal growth factor receptor and the calcium related signaling.

Authors :
Wu, Xia
Du, Juan
Song, Weitao
Cao, Meiping
Chen, Shude
Xia, Ruohong
Source :
PLoS ONE; 10/12/2018, Vol. 13 Issue 10, p1-27, 27p
Publication Year :
2018

Abstract

We have shown previously that a weak 50 Hz magnetic field (MF) invoked the actin-cytoskeleton, and provoked cell migration at the cell level, probably through activating the epidermal growth factor receptor (EGFR) related motility pathways. However, whether the MF also affects the microtubule (MT)-cytoskeleton is still unknown. In this article, we continuously investigate the effects of 0.4 mT, 50 Hz MF on the MT, and try to understand if the MT effects are also associated with the EGFR pathway as the actin-cytoskeleton effects were. Our results strongly suggest that the MF effects are similar to that of EGF stimulation on the MT cytoskeleton, showing that 1) the MF suppressed MT in multiple cell types including PC12 and FL; 2) the MF promoted the clustering of the EGFR at the protein and the cell levels, in a similar way of that EGF did but with higher sensitivity to PD153035 inhibition, and triggered EGFR phosphorylation on sites of Y1173 and S1046/1047; 3) these effects were strongly depending on the Ca<superscript>2+</superscript> signaling through the L-type calcium channel (LTCC) phosphorylation and elevation of the intracellular Ca<superscript>2+</superscript> level. Strong associations were observed between EGFR and the Ca<superscript>2+</superscript> signaling to regulate the MF-induced-reorganization of the cytoskeleton network, via phosphorylating the signaling proteins in the two pathways, including a significant MT protein, tau. These results strongly suggest that the MF activates the overall cytoskeleton in the absence of EGF, through a mechanism related to both the EGFR and the LTCC/Ca<superscript>2+</superscript> signaling pathways. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
19326203
Volume :
13
Issue :
10
Database :
Complementary Index
Journal :
PLoS ONE
Publication Type :
Academic Journal
Accession number :
132359298
Full Text :
https://doi.org/10.1371/journal.pone.0205569