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J Cell Physiol. 2019 Jun;234(6):7734-7741. doi: 10.1002/jcp.28102. Epub 2019 Jan 9.

S1P mediates human amniotic cells proliferation induced by a 50-Hz magnetic field exposure via ERK1/2 signaling pathway.

Qiu L1,2, Chen L2, Yang X2, Ye A3, Jiang W4, Sun W2,4,3.

Author information

1
Department of Preventive Health Care, Jinhua Hospital of Zhejiang University, Jinhua, China.
2
Bioelectromagnetics Key Laboratory, Zhejiang University School of Medicine, Hangzhou, China.
3
Department of Occupational Disease of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
4
Institute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou, China.

Abstract

Extremely low frequency electromagnetic field (ELF-EMF) is a kind of physical stimulus in public and occupational environment. Numerous studies have indicated that exposure of cells to ELF-EMF could promote cell proliferation. But the detailed mechanisms implicated in these proliferative processes remain unclear. In the present experiment, the possible roles of sphingosine-1-phosphate (S1P) in 50-Hz magnetic field (MF)-induced cell proliferation were investigated. Results showed that exposure of human amniotic (FL) cells to a 50-Hz MF with an intensity of 0.4 mT significantly enhanced ceramide metabolism, increased S1P production, activated extracellular signal regulated kinase 1/2 (ERK1/2), and promoted cell proliferation. All of these effects induced by MF exposure could be inhibited by SKI II, an inhibitor of sphingosine kinase (SphK). In addition, both the cell proliferative response and the ERK1/2 activation induced by MF exposure were blocked completely by U0126, a specific inhibitor of MEK (ERK kinases 1 and 2). Taken together, the findings in present study suggested that S1P mediated 50-Hz MF-induced cell proliferation via triggering ERK1/2 signal pathway.

KEYWORDS:

50-Hz magnetic field (MF) exposure; extracellular signal regulated kinase (ERK); proliferation; sphingosine-1-phosphate (S1P)

PMID:
30624774
DOI:
10.1002/jcp.28102

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