Egr1 mediated the neuronal differentiation induced by extremely low-frequency electromagnetic fields.

Life sciences · 2014 · Benefit · Low evidence

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BenefitLow evidencePaper 4701

hBM-MSCs exposed to ELF-EMF (50 Hz, 1 mT) for 8 days showed neuronal differentiation-associated changes, with Egr1 identified as a key transcription factor in ELF-EMF-induced neuronal differentiation. Transplantation of ELF-EMF-induced neurons significantly a…

Study snapshot

PublicationLife sciences · 2014
Study typeanimal
Reported directionBenefit
Evidence ratingLow

Abstract

AIM: There is a specific frequency of extremely low-frequency electromagnetic field (ELF-EMF) that promotes neuronal differentiation. Although several mechanisms are known to regulate ELF-EMF-induced neuronal differentiation, a key factor that mediates neurogenic potentials by the ELF-EMF is largely unknown. Also, the potential use of ELF-EMF exposure in cell transplantation assays is yet to be determined, including their possible use in ELF-EMF based therapy of neurological diseases. The aim of this study is to understand the underlying mechanisms that mediate ELF-EMF-induced neuronal differentiation and also to harness these mechanisms for cell transplantation assays. MAIN METHOD: Human bone marrow-mesenchymal stem cells (hBM-MSCs) were exposed to ELF-EMF (50 Hz frequency, 1mT intensity) for 8 days. The hBM-MSC derived neurons were then analyzed by general molecular biology techniques including immunofluorescence and quantitative RT-PCR. To assess changes in gene expression induced by ELF-EMF exposure, we analyzed the transcriptome of neuronal cells after an 8-day ELF-EMF exposure (50 Hz, 1 mT) and compared the transcriptional profiles to control cells. KEY FINDING: We found that early growth response protein 1 (Egr1) is one of the key transcription factors in ELF-EMF-induced neuronal differentiation. In addition, we show that transplantations of ELF-EMF-induced neurons significantly alleviate symptoms in mouse models of neurodegenerative disease. SIGNIFICANCE: These findings indicate that a specific transcriptional factor, Egr1, mediates ELF-EMF-induced neuronal differentiations, and demonstrate the promise of ELF-EMF based cell replacement therapies for neurodegenerative diseases.

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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 typeanimal
Effect directionbenefit
PopulationHuman bone marrow-mesenchymal stem cells (hBM-MSCs); mouse models of neurodegenerative disease (transplantation of ELF-EMF-induced neurons)
Sample sizeNot supplied
ExposureELF · 8 days (cell exposure)
Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

hBM-MSCs exposed to ELF-EMF (50 Hz, 1 mT) for 8 days showed neuronal differentiation-associated changes, with Egr1 identified as a key transcription factor in ELF-EMF-induced neuronal differentiation. Transplantation of ELF-EMF-induced neurons significantly alleviated symptoms in mouse models of neurodegenerative disease.

Outcomes measured

  • Neuronal differentiation of hBM-MSCs
  • Transcriptome/gene expression changes after ELF-EMF exposure
  • Egr1 involvement as a transcription factor in ELF-EMF-induced neuronal differentiation
  • Symptoms in mouse models of neurodegenerative disease after transplantation of ELF-EMF-induced neurons

Limitations

  • No sample size reported in abstract
  • Details of mouse models, transplantation protocol, and symptom measures not described in abstract
  • Exposure metrics beyond frequency, intensity, and duration (e.g., waveform, field uniformity) not provided
View raw extracted JSON
{
  "study_type": "animal",
  "exposure": {
    "band": "ELF",
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "8 days (cell exposure)"
  },
  "population": "Human bone marrow-mesenchymal stem cells (hBM-MSCs); mouse models of neurodegenerative disease (transplantation of ELF-EMF-induced neurons)",
  "sample_size": null,
  "outcomes": [
    "Neuronal differentiation of hBM-MSCs",
    "Transcriptome/gene expression changes after ELF-EMF exposure",
    "Egr1 involvement as a transcription factor in ELF-EMF-induced neuronal differentiation",
    "Symptoms in mouse models of neurodegenerative disease after transplantation of ELF-EMF-induced neurons"
  ],
  "main_findings": "hBM-MSCs exposed to ELF-EMF (50 Hz, 1 mT) for 8 days showed neuronal differentiation-associated changes, with Egr1 identified as a key transcription factor in ELF-EMF-induced neuronal differentiation. Transplantation of ELF-EMF-induced neurons significantly alleviated symptoms in mouse models of neurodegenerative disease.",
  "effect_direction": "benefit",
  "limitations": [
    "No sample size reported in abstract",
    "Details of mouse models, transplantation protocol, and symptom measures not described in abstract",
    "Exposure metrics beyond frequency, intensity, and duration (e.g., waveform, field uniformity) not provided"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "extremely low-frequency electromagnetic fields",
    "ELF-EMF",
    "50 Hz",
    "1 mT",
    "neuronal differentiation",
    "human bone marrow mesenchymal stem cells",
    "hBM-MSCs",
    "Egr1",
    "transcriptome",
    "cell transplantation",
    "neurodegenerative disease",
    "cell replacement therapy"
  ],
  "suggested_hubs": [
    {
      "slug": "elf-emf",
      "weight": 0.9,
      "reason": "Study uses extremely low-frequency EMF exposure (50 Hz, 1 mT) and examines biological effects."
    },
    {
      "slug": "stem-cells-regenerative-medicine",
      "weight": 0.75,
      "reason": "Uses hBM-MSCs differentiated into neurons and evaluates transplantation effects in mouse models."
    }
  ]
}
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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: 10.1016/j.lfs.2014.02.022
PubMed: 24603130

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