Electromagnetic fields affect transcript levels of apoptosis-related genes in embryonic stem cell-derived neural progenitor cells.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2005 · Mixed · Low evidence

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MixedLow evidencePaper 5167

Study snapshot

PublicationFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2005

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

Mouse embryonic stem (ES) cells were used as an experimental model to study the effects of electromagnetic fields (EMF). ES-derived nestin-positive neural progenitor cells were exposed to extremely low frequency EMF simulating power line magnetic fields at 50 Hz (ELF-EMF) and to radiofrequency EMF simulating the Global System for Mobile Communication (GSM) signals at 1.71 GHz (RF-EMF). Following EMF exposure, cells were analyzed for transcript levels of cell cycle regulatory, apoptosis-related, and neural-specific genes and proteins; changes in proliferation; apoptosis; and cytogenetic effects. Quantitative RT-PCR analysis revealed that ELF-EMF exposure to ES-derived neural cells significantly affected transcript levels of the apoptosis-related bcl-2, bax, and cell cycle regulatory "growth arrest DNA damage inducible" GADD45 genes, whereas mRNA levels of neural-specific genes were not affected. RF-EMF exposure of neural progenitor cells resulted in down-regulation of neural-specific Nurr1 and in up-regulation of bax and GADD45 mRNA levels. Short-term RF-EMF exposure for 6 h, but not for 48 h, resulted in a low and transient increase of DNA double-strand breaks. No effects of ELF- and RF-EMF on mitochondrial function, nuclear apoptosis, cell proliferation, and chromosomal alterations were observed. We may conclude that EMF exposure of ES-derived neural progenitor cells transiently affects the transcript level of genes related to apoptosis and cell cycle control. However, these responses are not associated with detectable changes of cell physiology, suggesting compensatory mechanisms at the translational and posttranslational level.

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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 directionmixed

PopulationMouse embryonic stem cell-derived (nestin-positive) neural progenitor cells

Sample sizeNot supplied

ExposureELF and RF · 1710 MHz · RF-EMF exposure assessed at 6 h and 48 h (short-term vs longer-term); ELF duration not stated

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

ELF-EMF (50 Hz) exposure significantly affected transcript levels of apoptosis-related bcl-2 and bax and the cell cycle regulatory gene GADD45, while neural-specific gene mRNA levels were not affected. RF-EMF (1.71 GHz GSM-like) exposure down-regulated neural-specific Nurr1 and up-regulated bax and GADD45 mRNA; 6 h RF exposure (but not 48 h) produced a low, transient increase in DNA double-strand breaks. No effects of ELF- or RF-EMF were observed on mitochondrial function, nuclear apoptosis, cell proliferation, or chromosomal alterations.

Outcomes measured

Transcript levels of apoptosis-related genes (bcl-2, bax)
Transcript levels of cell cycle regulatory gene GADD45
Transcript levels of neural-specific genes (including Nurr1)
Protein/gene expression analyses (cell cycle regulatory, apoptosis-related, neural-specific genes and proteins)
Cell proliferation
Apoptosis (nuclear apoptosis)
Cytogenetic effects / chromosomal alterations
DNA double-strand breaks
Mitochondrial function

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF and RF",
    "source": "power line magnetic fields (simulated) and GSM signals (simulated)",
    "frequency_mhz": 1710,
    "sar_wkg": null,
    "duration": "RF-EMF exposure assessed at 6 h and 48 h (short-term vs longer-term); ELF duration not stated"
  },
  "population": "Mouse embryonic stem cell-derived (nestin-positive) neural progenitor cells",
  "sample_size": null,
  "outcomes": [
    "Transcript levels of apoptosis-related genes (bcl-2, bax)",
    "Transcript levels of cell cycle regulatory gene GADD45",
    "Transcript levels of neural-specific genes (including Nurr1)",
    "Protein/gene expression analyses (cell cycle regulatory, apoptosis-related, neural-specific genes and proteins)",
    "Cell proliferation",
    "Apoptosis (nuclear apoptosis)",
    "Cytogenetic effects / chromosomal alterations",
    "DNA double-strand breaks",
    "Mitochondrial function"
  ],
  "main_findings": "ELF-EMF (50 Hz) exposure significantly affected transcript levels of apoptosis-related bcl-2 and bax and the cell cycle regulatory gene GADD45, while neural-specific gene mRNA levels were not affected. RF-EMF (1.71 GHz GSM-like) exposure down-regulated neural-specific Nurr1 and up-regulated bax and GADD45 mRNA; 6 h RF exposure (but not 48 h) produced a low, transient increase in DNA double-strand breaks. No effects of ELF- or RF-EMF were observed on mitochondrial function, nuclear apoptosis, cell proliferation, or chromosomal alterations.",
  "effect_direction": "mixed",
  "limitations": [],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "embryonic stem cells",
    "neural progenitor cells",
    "ELF-EMF",
    "50 Hz",
    "RF-EMF",
    "GSM",
    "1.71 GHz",
    "apoptosis-related genes",
    "bcl-2",
    "bax",
    "GADD45",
    "Nurr1",
    "DNA double-strand breaks",
    "mitochondrial function",
    "cell proliferation",
    "chromosomal alterations"
  ],
  "suggested_hubs": [
    {
      "slug": "occupational-exposure",
      "weight": 0.2,
      "reason": "Includes simulated power line (50 Hz) magnetic field exposure, relevant to ELF contexts."
    }
  ]
}

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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: 10.1096/fj.04-3549fje
PubMed: 16116041

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