Endogenous Ca 2+ release was involved in 50-Hz MF-induced proliferation via Akt-SK1 signal cascade in human amniotic epithelial cells

Electromagnetic biology and medicine · 2022 · Benefit · Low evidence

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BenefitLow evidencePaper 907

Study snapshot

PublicationElectromagnetic biology and medicine · 2022

Study typein_vitro

Reported directionBenefit

Evidence ratingLow

Abstract

Endogenous Ca 2+ release was involved in 50-Hz MF-induced proliferation via Akt-SK1 signal cascade in human amniotic epithelial cells An-Fang Ye, Xiao-Chen Liu, Liang-Jing Chen, Yong-Peng Xia, Xiao-Bo Yang, Wen-Jun Sun. Endogenous Ca 2+ release was involved in 50-Hz MF-induced proliferation via Akt-SK1 signal cascade in human amniotic epithelial cells. Electromagn Biol Med. 2022 Feb 7;1-10. doi: 10.1080/15368378.2022.2031211. Abstract The mechanism underlying the biological effects caused by an extremely low-frequency electromagnetic field (ELF-EMF) is still unclear. Previously, we found that L-type calcium channel and sphingosine kinase 1 (SK1) were involved in 50-Hz MF exposure-induced cell proliferation. In the present study, the role of intracellular Ca2+ and signal molecules related to SK1 in cell proliferation induced by 50-Hz MF was investigated in human amniotic epithelial (FL) cells. Results showed that the intracellular Ca2+ chelator, BAPTA, could completely inhibit 50-Hz MF-induced cell proliferation, whereas NIF, the inhibitor of L-type calcium channel, only partly blocked it. When cells were cultured in calcium-free medium, MF exposure also increased intracellular Ca2+, activated SK1 and promoted cell proliferation although all of those increasing levels were lower than those in complete medium. Moreover, MF-activated SK1 could be completely inhibited by BAPTA, and MF-induced cell proliferation was abolished by SKI II, the specific inhibitor of SK1. Additionally, a 50-Hz MF exposure did not affect the activation of ERK and PKCα under the condition of calcium-free medium, but activated the Akt, which could be precluded entirely by BAPTA, but not be inhibited by NIF. Treatment of FL cells with LY294002, the inhibitor of Akt, could delete the MF-induced SK1 activation under the condition of calcium-free medium. Based on the data from the present experiment, it is concluded that endogenous Ca2+ release was involved in 50-Hz MF-induced cell proliferation via Akt-SK1 signal cascade. pubmed.ncbi.nlm.nih.gov

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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 directionbenefit

PopulationHuman amniotic epithelial (FL) cells

Sample sizeNot supplied

ExposureELF · 0.05 MHz

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

In human amniotic epithelial (FL) cells, 50-Hz magnetic field exposure increased intracellular Ca2+, activated SK1, and promoted cell proliferation. MF-induced proliferation was completely inhibited by the intracellular Ca2+ chelator BAPTA and abolished by the SK1 inhibitor SKI II; the L-type calcium channel inhibitor NIF only partly blocked proliferation. Under calcium-free medium, MF exposure still increased intracellular Ca2+, activated SK1, and promoted proliferation (to a lesser extent), and Akt activation was observed and could be prevented by BAPTA; Akt inhibition (LY294002) prevented MF-induced SK1 activation in calcium-free medium.

Outcomes measured

Cell proliferation
Intracellular Ca2+ levels
SK1 activation
Akt activation
ERK activation
PKCα activation

Limitations

Exposure intensity (e.g., magnetic flux density) not reported in the abstract
Exposure duration not reported in the abstract
In vitro cell model; generalizability to humans/health outcomes is unclear from the abstract
Sample size and replication details not provided in the abstract

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": null,
    "frequency_mhz": 0.05,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human amniotic epithelial (FL) cells",
  "sample_size": null,
  "outcomes": [
    "Cell proliferation",
    "Intracellular Ca2+ levels",
    "SK1 activation",
    "Akt activation",
    "ERK activation",
    "PKCα activation"
  ],
  "main_findings": "In human amniotic epithelial (FL) cells, 50-Hz magnetic field exposure increased intracellular Ca2+, activated SK1, and promoted cell proliferation. MF-induced proliferation was completely inhibited by the intracellular Ca2+ chelator BAPTA and abolished by the SK1 inhibitor SKI II; the L-type calcium channel inhibitor NIF only partly blocked proliferation. Under calcium-free medium, MF exposure still increased intracellular Ca2+, activated SK1, and promoted proliferation (to a lesser extent), and Akt activation was observed and could be prevented by BAPTA; Akt inhibition (LY294002) prevented MF-induced SK1 activation in calcium-free medium.",
  "effect_direction": "benefit",
  "limitations": [
    "Exposure intensity (e.g., magnetic flux density) not reported in the abstract",
    "Exposure duration not reported in the abstract",
    "In vitro cell model; generalizability to humans/health outcomes is unclear from the abstract",
    "Sample size and replication details not provided in the abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "ELF-EMF",
    "50-Hz magnetic field",
    "human amniotic epithelial cells",
    "FL cells",
    "cell proliferation",
    "intracellular calcium",
    "BAPTA",
    "L-type calcium channel",
    "NIF",
    "sphingosine kinase 1",
    "SK1",
    "SKI II",
    "Akt",
    "LY294002",
    "signal cascade"
  ],
  "suggested_hubs": [
    {
      "slug": "occupational-exposure",
      "weight": 0.25,
      "reason": "Study involves 50-Hz ELF magnetic field exposure, which is commonly discussed in occupational/ELF exposure contexts, though no specific occupational setting is stated."
    }
  ]
}

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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: 10.1080/15368378.2022.2031211
PubMed: 35129008

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