Extremely low frequency electromagnetic fields modulate expression of inducible nitric oxide synthase, endothelial nitric oxide synthase and cyclooxygenase-2 in the human keratinocyte cell line HaCat: potential therapeutic effects in wound healing.

The British journal of dermatology · 2010 · Mixed · Low evidence

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MixedLow evidencePaper 4413

Compared with unexposed controls, ELF-EMF exposure increased iNOS and eNOS expression, NOS activities, NO production, AP-1 expression, and cell proliferation rate. ELF-EMF exposure decreased COX-2 expression, PGE2 production, catalase activity, and O2− produc…

Study snapshot

PublicationThe British journal of dermatology · 2010

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

BACKGROUND: Extremely low frequency (ELF) electromagnetic fields (EMF) are known to produce a variety of biological effects. Clinical studies are ongoing using EMF in healing of bone fractures and skin wounds. However, little is known about the mechanisms of action of ELF-EMF. Several studies have demonstrated that expression and regulation of nitric oxide synthase (NOS) and cyclooxygenase-2 (COX-2) are vital for wound healing; however, no reports have demonstrated a direct action of ELF-EMF in the modulation of these inflammatory molecules in human keratinocytes. OBJECTIVES: The present study analysed the effect of ELF-EMF on the human keratinocyte cell line HaCaT in order to assess the mechanisms of action of ELF-EMF and to provide further support for their therapeutic use in wound healing. METHODS: Exposed HaCaT cells were compared with unexposed control cells. At different exposure times, expression of inducible NOS (iNOS), endothelial NOS (eNOS) and COX-2 was evaluated by Western blot analysis. Modulation of iNOS and eNOS was monitored by evaluation of NOS activities, production of nitric oxide (NO) and O(2)(-) and expression of activator protein 1 (AP-1). In addition, catalase activity and prostaglandin (PG) E(2) production were determined. Effects of ELF-EMF on cell growth and viability were monitored. RESULTS: The exposure of HaCaT cells to ELF-EMF increased iNOS and eNOS expression levels. These ELF-EMF-dependent increased expression levels were paralled by increased NOS activities, and increased NO production. In addition, higher levels of AP-1 expression as well as a higher cell proliferation rate were associated with ELF-EMF exposure. In contrast, ELF-EMF decreased COX-2 expression, PGE(2) production, catalase activity and O(2)(-) production. CONCLUSIONS: Mediators of inflammation, such as reactive nitrogen and PGE(2), and keratinocyte proliferation are critical for the tissue regenerative processes. The ability of ELF-EMF to upmodulate NOS activities, thus nitrogen intermediates, as well as cell proliferation, and to downregulate COX-2 expression and the downstream intermediate PGE(2), highlights the potential therapeutic role of ELF-EMF in wound healing processes.

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 directionmixed

PopulationHuman keratinocyte cell line HaCaT

Sample sizeNot supplied

ExposureELF

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Outcomes measured

iNOS expression
eNOS expression
COX-2 expression
NOS activity
Nitric oxide (NO) production
Superoxide (O2−) production
Activator protein 1 (AP-1) expression
Catalase activity
Prostaglandin E2 (PGE2) production
Cell growth/proliferation
Cell viability

Limitations

In vitro study in a single human keratinocyte cell line (HaCaT), limiting generalizability to in vivo wound healing.
Exposure parameters (e.g., frequency, field strength, waveform, and duration) are not provided in the abstract.
Sample size/replication and statistical details are not reported in the abstract.
Outcomes are molecular/biochemical markers rather than clinical wound-healing endpoints.

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human keratinocyte cell line HaCaT",
  "sample_size": null,
  "outcomes": [
    "iNOS expression",
    "eNOS expression",
    "COX-2 expression",
    "NOS activity",
    "Nitric oxide (NO) production",
    "Superoxide (O2−) production",
    "Activator protein 1 (AP-1) expression",
    "Catalase activity",
    "Prostaglandin E2 (PGE2) production",
    "Cell growth/proliferation",
    "Cell viability"
  ],
  "main_findings": "Compared with unexposed controls, ELF-EMF exposure increased iNOS and eNOS expression, NOS activities, NO production, AP-1 expression, and cell proliferation rate. ELF-EMF exposure decreased COX-2 expression, PGE2 production, catalase activity, and O2− production; effects on cell viability were monitored but not reported in the abstract.",
  "effect_direction": "mixed",
  "limitations": [
    "In vitro study in a single human keratinocyte cell line (HaCaT), limiting generalizability to in vivo wound healing.",
    "Exposure parameters (e.g., frequency, field strength, waveform, and duration) are not provided in the abstract.",
    "Sample size/replication and statistical details are not reported in the abstract.",
    "Outcomes are molecular/biochemical markers rather than clinical wound-healing endpoints."
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "extremely low frequency",
    "ELF-EMF",
    "electromagnetic fields",
    "keratinocytes",
    "HaCaT",
    "wound healing",
    "iNOS",
    "eNOS",
    "COX-2",
    "nitric oxide",
    "PGE2",
    "AP-1",
    "inflammation",
    "cell proliferation"
  ],
  "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: 10.1111/j.1365-2133.2009.09527.x
PubMed: 19799606

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