Involvement of calcium in 50‐Hz magnetic field‐induced activation of sphingosine kinase 1 signaling pathway

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 a...

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Veröffentlicht in:Bioelectromagnetics 2019-04, Vol.40 (3), p.180-187
Hauptverfasser: Yang, Xiaobo, Ye, Anfang, Chen, Liangjing, Xia, Yongpeng, Jiang, Wei, Sun, Wenjun
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container_issue 3
container_start_page 180
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creator Yang, Xiaobo
Ye, Anfang
Chen, Liangjing
Xia, Yongpeng
Jiang, Wei
Sun, Wenjun
description 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 Ca2+ which was dependent on the L‐type calcium channel, and induced Ca2+‐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 Ca2+ 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.
doi_str_mv 10.1002/bem.22181
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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 Ca2+ which was dependent on the L‐type calcium channel, and induced Ca2+‐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 Ca2+ 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. 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subjects 50‐Hz magnetic field (MF)
Activation
Calcium
Calcium (extracellular)
Calcium (intracellular)
Calcium ions
Cell proliferation
Exposure
extracellular regulated protein kinase (ERK)
Extracellular signal-regulated kinase
Inhibitors
Intracellular
intracellular Ca2
Kinases
Magnetic fields
Phosphorylation
Protein kinase C
protein kinase Cα (PKCα)
Proteins
Signal transduction
Signaling
Sphingosine kinase
Sphingosine kinase 1 (SK1)
title Involvement of calcium in 50‐Hz magnetic field‐induced activation of sphingosine kinase 1 signaling pathway
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