Autophagy is modulated in human neuroblastoma cells through direct exposition to low frequency electromagnetic fields.

Journal of cellular physiology · 2014 · Benefit · Low evidence

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BenefitLow evidencePaper 4695

Study snapshot

PublicationJournal of cellular physiology · 2014

Study typein_vitro

Reported directionBenefit

Evidence ratingLow

Abstract

In neurogenerative diseases, comprising Alzheimer's (AD), functional alteration in autophagy is considered one of the pathological hallmarks and a promising therapeutic target. Epidemiological investigations on the possible causes undergoing these diseases have suggested that electromagnetic fields (EMF) exposition can contribute to their etiology. On the other hand, EMF have therapeutic implications in reactivating neuronal functionality. To partly clarify this dualism, the effect of low-frequency EMF (LF-EMF) on the modulation of autophagy was investigated in human neuroblastoma SH-SY5Y cells, which were also subsequently exposed to Aβ peptides, key players in AD. The results primarily point that LF-EMF induce a significant reduction of microRNA 30a (miR-30a) expression with a concomitant increase of Beclin1 transcript (BECN1) and its corresponding protein. Furthermore, LF-EMF counteract the induced miR-30a up-regulation in the same cells transfected with miR-30a mimic precursor molecules and, on the other side, rescue Beclin1 expression after BECN1 siRNA treatment. The expression of autophagy-related markers (ATG7 and LC3B-II) as well as the dynamics of autophagosome formation were also visualized after LF-EMF exposition. Finally, different protocols of repeated LF-EMF treatments were assayed to contrast the effects of Aβ peptides in vitro administration. Overall, this research demonstrates, for the first time, that specific LF-EMF treatments can modulate in vitro the expression of a microRNA sequence, which in turn affects autophagy via Beclin1 expression. Taking into account the pivotal role of autophagy in the clearance of protein aggregates within the cells, our results indicate a potential cytoprotective effect exerted by LF-EMF in neurodegenerative diseases such as AD. J. Cell. Physiol. 229: 1776-1786, 2014. © 2014 Wiley Periodicals, Inc.

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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 neuroblastoma SH-SY5Y cells (in vitro), including conditions with subsequent Aβ peptide exposure

Sample sizeNot supplied

ExposureELF

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

LF-EMF exposure was associated with reduced miR-30a expression and increased Beclin1 (BECN1) transcript and protein in SH-SY5Y cells. LF-EMF counteracted miR-30a up-regulation after miR-30a mimic transfection and rescued Beclin1 expression after BECN1 siRNA treatment; autophagy markers (ATG7, LC3B-II) and autophagosome formation were visualized after exposure. Repeated LF-EMF protocols were tested to contrast effects of Aβ peptides in vitro, and the authors interpret findings as indicating a potential cytoprotective effect via autophagy modulation.

Outcomes measured

microRNA 30a (miR-30a) expression
Beclin1 transcript (BECN1) and protein expression
Autophagy-related markers (ATG7, LC3B-II)
Autophagosome formation dynamics
Response to Aβ peptide administration under repeated LF-EMF treatment protocols

Limitations

In vitro cell model (SH-SY5Y); findings may not translate to humans or clinical neurodegenerative disease
LF-EMF exposure parameters (e.g., frequency, field strength, duration) not provided in the abstract
Sample size and quantitative effect sizes not reported in the abstract
Aβ peptide protocols and outcomes of the repeated LF-EMF treatment comparisons are not detailed in the abstract

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human neuroblastoma SH-SY5Y cells (in vitro), including conditions with subsequent Aβ peptide exposure",
  "sample_size": null,
  "outcomes": [
    "microRNA 30a (miR-30a) expression",
    "Beclin1 transcript (BECN1) and protein expression",
    "Autophagy-related markers (ATG7, LC3B-II)",
    "Autophagosome formation dynamics",
    "Response to Aβ peptide administration under repeated LF-EMF treatment protocols"
  ],
  "main_findings": "LF-EMF exposure was associated with reduced miR-30a expression and increased Beclin1 (BECN1) transcript and protein in SH-SY5Y cells. LF-EMF counteracted miR-30a up-regulation after miR-30a mimic transfection and rescued Beclin1 expression after BECN1 siRNA treatment; autophagy markers (ATG7, LC3B-II) and autophagosome formation were visualized after exposure. Repeated LF-EMF protocols were tested to contrast effects of Aβ peptides in vitro, and the authors interpret findings as indicating a potential cytoprotective effect via autophagy modulation.",
  "effect_direction": "benefit",
  "limitations": [
    "In vitro cell model (SH-SY5Y); findings may not translate to humans or clinical neurodegenerative disease",
    "LF-EMF exposure parameters (e.g., frequency, field strength, duration) not provided in the abstract",
    "Sample size and quantitative effect sizes not reported in the abstract",
    "Aβ peptide protocols and outcomes of the repeated LF-EMF treatment comparisons are not detailed in the abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "low-frequency electromagnetic fields",
    "LF-EMF",
    "ELF-EMF",
    "autophagy",
    "microRNA",
    "miR-30a",
    "Beclin1",
    "BECN1",
    "ATG7",
    "LC3B-II",
    "autophagosome",
    "SH-SY5Y",
    "neuroblastoma",
    "Alzheimer's disease",
    "Aβ peptides"
  ],
  "suggested_hubs": []
}

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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/jcp.24631
PubMed: 24676932

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