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Involvement of calcium in 50‐Hz magnetic field‐induced activation of sphingosine kinase 1 signaling pathway
Author(s) -
Yang Xiaobo,
Ye Anfang,
Chen Liangjing,
Xia Yongpeng,
Jiang Wei,
Sun Wenjun
Publication year - 2019
Publication title -
bioelectromagnetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.435
H-Index - 81
eISSN - 1521-186X
pISSN - 0197-8462
DOI - 10.1002/bem.22181
Subject(s) - protein kinase c , sphingosine , phosphorylation , mapk/erk pathway , sphingosine kinase 1 , microbiology and biotechnology , kinase , sphingosine kinase , p38 mitogen activated protein kinases , bioelectromagnetics , signal transduction , chemistry , mitogen activated protein kinase 3 , sphingosine 1 phosphate , biology , biochemistry , physics , receptor , magnetic field , quantum mechanics
Previously, we found that exposure to a 50‐Hz magnetic field (MF) could induce human amniotic epithelial (FL) cell proliferation and sphingosine kinase 1 (SK1) activation, but the mechanism was not clearly understood. In the present study, the possible signaling pathways which were involved in SK1 activation induced by 50‐Hz MF exposure were investigated. Results showed that MF exposure increased intracellular Ca 2+ which was dependent on the L‐type calcium channel, and induced Ca 2+ ‐dependent phosphorylation of extracellular regulated protein kinase (ERK), SK1, and protein kinase C α (PKCα). Also, treatment with U0126, an inhibitor of ERK, could block MF‐induced SK1 phosphorylation, but had no effect on PKCα phosphorylation. Also, the inhibitor of PKCα, Gö6976, had no effect on MF‐induced SK1 activation in FL cells. In addition, the activation of ERK and PKCα could be abolished by SKI II, the inhibitor of SK1. In conclusion, the intracellular Ca 2+ mediated the 50‐Hz MF‐induced SK1 activation which enhanced PKCα phosphorylation, and there might be a feedback mechanism between SK1 and ERK activation in responding to MF exposure in FL cells. Bioelectromagnetics. 9999:XX–XX, 2019. © 2019 Bioelectromagnetics Society.