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

2019 · Mixed · Low evidence

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MixedLow evidencePaper 1874

50-Hz magnetic field exposure increased intracellular Ca2+ in FL cells in an L-type calcium channel-dependent manner and induced Ca2+-dependent phosphorylation of ERK, SK1, and PKCα. ERK inhibition (U0126) blocked MF-induced SK1 phosphorylation, while PKCα in…

Study snapshot

Publicationmanual · 2019
Study typein_vitro
Reported directionMixed
Evidence ratingLow

Abstract

Involvement of calcium in 50-Hz magnetic field-induced activation of sphingosine kinase 1 signaling pathway Yang X, Ye A, Chen L, Xia Y, Jiang W, Sun. Involvement of calcium in 50-Hz magnetic field-induced activation of sphingosine kinase 1 signaling pathway. Bioelectromagnetics. 2019 Apr;40(3):180-187. doi: 10.1002/bem.22181. Abstract 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. ncbi.nlm.nih.gov

Machine Enhanced Logic

AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro
Effect directionmixed
PopulationHuman amniotic epithelial (FL) cells
Sample sizeNot supplied
ExposureELF · 0.05 MHz
Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

50-Hz magnetic field exposure increased intracellular Ca2+ in FL cells in an L-type calcium channel-dependent manner and induced Ca2+-dependent phosphorylation of ERK, SK1, and PKCα. ERK inhibition (U0126) blocked MF-induced SK1 phosphorylation, while PKCα inhibition (Gö6976) did not affect MF-induced SK1 activation; SK1 inhibition (SKI II) abolished ERK and PKCα activation.

Outcomes measured

  • Intracellular Ca2+ levels
  • L-type calcium channel involvement
  • ERK phosphorylation
  • SK1 phosphorylation/activation
  • PKCα phosphorylation
  • Effects of inhibitors (U0126, Gö6976, SKI II) on signaling responses

Limitations

  • Exposure duration not reported in abstract
  • Magnetic field intensity not reported in abstract
  • In vitro cell model; generalizability to humans not addressed in abstract
  • Sample size and replication details not reported in abstract
View raw extracted JSON
{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": "magnetic field",
    "frequency_mhz": 0.05,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human amniotic epithelial (FL) cells",
  "sample_size": null,
  "outcomes": [
    "Intracellular Ca2+ levels",
    "L-type calcium channel involvement",
    "ERK phosphorylation",
    "SK1 phosphorylation/activation",
    "PKCα phosphorylation",
    "Effects of inhibitors (U0126, Gö6976, SKI II) on signaling responses"
  ],
  "main_findings": "50-Hz magnetic field exposure increased intracellular Ca2+ in FL cells in an L-type calcium channel-dependent manner and induced Ca2+-dependent phosphorylation of ERK, SK1, and PKCα. ERK inhibition (U0126) blocked MF-induced SK1 phosphorylation, while PKCα inhibition (Gö6976) did not affect MF-induced SK1 activation; SK1 inhibition (SKI II) abolished ERK and PKCα activation.",
  "effect_direction": "mixed",
  "limitations": [
    "Exposure duration not reported in abstract",
    "Magnetic field intensity not reported in abstract",
    "In vitro cell model; generalizability to humans not addressed in abstract",
    "Sample size and replication details not reported in abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "50-Hz magnetic field",
    "ELF",
    "calcium",
    "L-type calcium channel",
    "sphingosine kinase 1",
    "SK1",
    "ERK",
    "PKCα",
    "FL cells",
    "signal transduction"
  ],
  "suggested_hubs": [
    {
      "slug": "occupational-exposure",
      "weight": 0.2,
      "reason": "Study involves 50-Hz magnetic field exposure (common in power-frequency environments), though no occupational setting is described."
    }
  ]
}
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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1002/bem.22181
PubMed: Not supplied

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