Electromagnetic fields (EMFs) and adenosine receptors modulate prostaglandin E(2) and cytokine release in human osteoarthritic synovial fibroblasts.

Journal of cellular physiology · 2012 · Benefit · Low evidence

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BenefitLow evidencePaper 4553

EMF exposure increased A2A and A3 adenosine receptor levels and was associated with changes in cAMP, suggesting functional receptor activity. In IL-1β-treated osteoarthritic synovial fibroblasts, EMFs inhibited release of PGE2, IL-6, and IL-8 and stimulated r…

Study snapshot

PublicationJournal of cellular physiology · 2012

Study typein_vitro

Reported directionBenefit

Evidence ratingLow

Abstract

Synovial fibroblasts (SFs) contribute to the development of osteoarthritis (OA) by the secretion of a wide range of pro-inflammatory mediators, including cytokines and lipid mediators of inflammation. Previous studies suggest that electromagnetic fields (EMFs) may represent a potential therapeutic approach to limit cartilage degradation and control inflammation associated to OA, and that they may act through the adenosine pathway. Therefore, we investigated whether EMFs might modulate inflammatory activities of human SFs from OA patients (OASFs) treated with interleukin-1β (IL-1β), and the possible involvement of adenosine receptors (ARs) in mediating EMF effects. EMF exposure induced a selective increase in A(2A) and A(3) ARs. These increases were associated to changes in cAMP levels, indicating that ARs were functionally active also in EMF-exposed cells. Functional data obtained in the presence of selective A(2A) and A(3) adenosine agonists and antagonists showed that EMFs inhibit the release of prostaglandin E(2) (PGE(2)) and the proinflammatory cytokines interleukin-6 (IL-6) and interleukin-8 (IL-8), while stimulating the release of interleukin-10 (IL-10), an antinflammatory cytokine. These effects seem to be mediated by the EMF-induced upregulation of A(2A) and A(3) ARs. No effects of EMFs or ARs have been observed on matrix degrading enzyme production. In conclusion, this study shows that EMFs display anti-inflammatory effects in human OASFs, and that these EMF-induced effects are in part mediated by the adenosine pathway, specifically by the A(2A) and A(3) AR activation. Taken together, these results open new clinical perspectives to the control of inflammation associated to joint diseases.

Machine Enhanced Logic

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 osteoarthritic synovial fibroblasts (from osteoarthritis patients) treated with interleukin-1β (IL-1β)

Sample sizeNot supplied

ExposureNot supplied

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

Outcomes measured

A2A adenosine receptor expression
A3 adenosine receptor expression
cAMP levels
Prostaglandin E2 (PGE2) release
Interleukin-6 (IL-6) release
Interleukin-8 (IL-8) release
Interleukin-10 (IL-10) release
Matrix degrading enzyme production

Limitations

No EMF exposure parameters (e.g., frequency, intensity, duration, SAR) reported in the abstract.
In vitro study in synovial fibroblasts; clinical relevance cannot be determined from the abstract.
Sample size not reported in the abstract.

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": null,
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human osteoarthritic synovial fibroblasts (from osteoarthritis patients) treated with interleukin-1β (IL-1β)",
  "sample_size": null,
  "outcomes": [
    "A2A adenosine receptor expression",
    "A3 adenosine receptor expression",
    "cAMP levels",
    "Prostaglandin E2 (PGE2) release",
    "Interleukin-6 (IL-6) release",
    "Interleukin-8 (IL-8) release",
    "Interleukin-10 (IL-10) release",
    "Matrix degrading enzyme production"
  ],
  "main_findings": "EMF exposure increased A2A and A3 adenosine receptor levels and was associated with changes in cAMP, suggesting functional receptor activity. In IL-1β-treated osteoarthritic synovial fibroblasts, EMFs inhibited release of PGE2, IL-6, and IL-8 and stimulated release of IL-10; no effects were observed on matrix degrading enzyme production.",
  "effect_direction": "benefit",
  "limitations": [
    "No EMF exposure parameters (e.g., frequency, intensity, duration, SAR) reported in the abstract.",
    "In vitro study in synovial fibroblasts; clinical relevance cannot be determined from the abstract.",
    "Sample size not reported in the abstract."
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electromagnetic fields",
    "EMF",
    "osteoarthritis",
    "synovial fibroblasts",
    "adenosine receptors",
    "A2A",
    "A3",
    "cAMP",
    "prostaglandin E2",
    "PGE2",
    "IL-6",
    "IL-8",
    "IL-10",
    "inflammation"
  ],
  "suggested_hubs": [
    {
      "slug": "other",
      "weight": 0.2,
      "reason": "In vitro study of EMF effects on inflammatory mediator release in osteoarthritic synovial fibroblasts; not clearly tied to common exposure hubs (e.g., mobile, Wi‑Fi, occupational) in the abstract."
    }
  ]
}

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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.22981
PubMed: 21830213

Read the original paper →

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