Electromagnetic field treatment increases purinergic receptor P2X7 expression and activates its downstream Akt/GSK3β/β-catenin axis in mesenchymal stem cells under osteogenic induction.

Stem cell research & therapy · 2019 · Benefit · Low evidence

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BenefitLow evidencePaper 5565

EMF treatment increased P2X7 expression in h-MSCs during osteogenic induction (not in regular culture) and increased activity of the Akt/GSK3β/β-catenin axis. Inhibition of P2X7 or PI3K/Akt partially reduced EMF pro-osteogenic effects, while adding a P2X7 ago…

Study snapshot

PublicationStem cell research & therapy · 2019
Study typeanimal
Reported directionBenefit
Evidence ratingLow

Abstract

BACKGROUND: Imbalance in bone formation and resorption is a crucial component of the pathological process leading to osteoporosis. Electromagnetic fields (EMFs) have been reported to be beneficial to osteogenesis, although the exact mechanism has not been fully clarified. Purinergic receptor P2X7 is expressed in osteoblasts and is reported to participate in the regulation of bone metabolism. OBJECTIVES: To elucidate the link between EMFs and P2X7 expression and investigate its potential as a novel therapeutic target in osteoporosis. METHOD: We investigated the effect of EMFs on P2X7 expression and downstream signaling in human bone marrow mesenchymal stem cells (h-MSCs). We also established an ovariectomized (OVX) osteoporosis rat model to evaluate the therapeutic efficacy of combining EMFs with P2X7 agonists. RESULTS: EMF treatment increased P2X7 expression in h-MSCs under conditions of osteogenic induction but not under regular culture conditions. P2X7 or PI3K/Akt inhibition partially inhibited the pro-osteogenic effect of EMF and lowered the EMF-stimulated activity of the Akt/GSK3β/β-catenin axis. No additive effect of this suppression was observed following simultaneous inhibition of P2X7 and PI3K/Akt. EMF treatment in the presence of a P2X7 agonist had a greater effect in increasing osteogenic marker expression than that of EMF treatment alone. In the OVX osteoporosis model, the therapeutic efficacy of combining EMFs with P2X7 agonists was superior to that of EMF treatment alone. CONCLUSIONS: EMF treatment increases P2X7 expression by h-MSCs during osteogenic differentiation, leading to activation of the Akt/GSK3β/β-catenin axis, which promotes the osteogenesis. Our findings also indicate that combined EMF and P2X7 agonist treatment may be an effective novel strategy for osteoporosis therapy.

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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 (h-MSCs) under osteogenic induction (in vitro) and ovariectomized (OVX) osteoporosis rat model (in vivo)
Sample sizeNot supplied
ExposureNot supplied
Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

EMF treatment increased P2X7 expression in h-MSCs during osteogenic induction (not in regular culture) and increased activity of the Akt/GSK3β/β-catenin axis. Inhibition of P2X7 or PI3K/Akt partially reduced EMF pro-osteogenic effects, while adding a P2X7 agonist with EMF increased osteogenic marker expression more than EMF alone; in OVX rats, combined EMF + P2X7 agonist was more efficacious than EMF alone.

Outcomes measured

  • P2X7 receptor expression
  • Akt/GSK3β/β-catenin signaling axis activity
  • Osteogenic marker expression / osteogenesis
  • Therapeutic efficacy in OVX osteoporosis rat model (combined EMF + P2X7 agonist vs EMF alone)

Limitations

  • EMF exposure parameters (e.g., frequency, intensity, duration) are not provided in the abstract.
  • Sample sizes and quantitative effect estimates are not reported in the abstract.
  • Mechanistic and therapeutic findings are based on in vitro h-MSC experiments and an animal (OVX rat) model; human clinical outcomes are not assessed in the abstract.
View raw extracted JSON
{
  "study_type": "animal",
  "exposure": {
    "band": null,
    "source": "other",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human bone marrow mesenchymal stem cells (h-MSCs) under osteogenic induction (in vitro) and ovariectomized (OVX) osteoporosis rat model (in vivo)",
  "sample_size": null,
  "outcomes": [
    "P2X7 receptor expression",
    "Akt/GSK3β/β-catenin signaling axis activity",
    "Osteogenic marker expression / osteogenesis",
    "Therapeutic efficacy in OVX osteoporosis rat model (combined EMF + P2X7 agonist vs EMF alone)"
  ],
  "main_findings": "EMF treatment increased P2X7 expression in h-MSCs during osteogenic induction (not in regular culture) and increased activity of the Akt/GSK3β/β-catenin axis. Inhibition of P2X7 or PI3K/Akt partially reduced EMF pro-osteogenic effects, while adding a P2X7 agonist with EMF increased osteogenic marker expression more than EMF alone; in OVX rats, combined EMF + P2X7 agonist was more efficacious than EMF alone.",
  "effect_direction": "benefit",
  "limitations": [
    "EMF exposure parameters (e.g., frequency, intensity, duration) are not provided in the abstract.",
    "Sample sizes and quantitative effect estimates are not reported in the abstract.",
    "Mechanistic and therapeutic findings are based on in vitro h-MSC experiments and an animal (OVX rat) model; human clinical outcomes are not assessed in the abstract."
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electromagnetic fields",
    "EMF",
    "osteogenesis",
    "osteoporosis",
    "mesenchymal stem cells",
    "P2X7",
    "PI3K/Akt",
    "GSK3β",
    "β-catenin",
    "ovariectomized rat"
  ],
  "suggested_hubs": [
    {
      "slug": "animal-studies",
      "weight": 0.78,
      "reason": "Includes an ovariectomized osteoporosis rat model evaluating EMF-based therapy."
    }
  ]
}
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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: 10.1186/s13287-019-1497-1
PubMed: 31864409

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