Exposure of B-lineage lymphoid cells to low energy electromagnetic fields stimulates Lyn kinase.

The Journal of biological chemistry · 1995 · Mixed · Low evidence

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MixedLow evidencePaper 5437

Study snapshot

PublicationThe Journal of biological chemistry · 1995

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

Here, we present evidence that exposure of B-lineage lymphoid cells to low energy electromagnetic fields (EMF) stimulates the protein tyrosine kinases Lyn and Syk, results in tyrosine phosphorylation of multiple electrophoretically distinct substrates, and leads to downstream activation of protein kinase C (PKC). EMF exposure enhances protein tyrosine phosphorylation in Syk deficient but not in Lyn-deficient B-lineage lymphoid cells and stimulates Lyn kinase activity in wild-type as well as Syk-deficient B-lineage lymphoid cells. These results indicate that activation of Lyn kinase is sufficient and mandatory for EMF-induced tyrosine phosphorylation in B-lineage lymphoid cells. The PKC activity increases later than the Lyn activity and pretreatment with the PTK inhibitors genistein or herbimycin A abrogates the EMF-induced PKC signal. Thus, stimulation of Lyn is a proximal and mandatory step in EMF-induced activation of PKC in B-lineage lymphoid cells. Our observations prompt the hypothesis that a delicate growth regulatory balance might be altered in B-lineage lymphoid cells by EMF-induced activation of Lyn.

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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 directionmixed

PopulationB-lineage lymphoid cells (including Lyn-deficient and Syk-deficient cells)

Sample sizeNot supplied

ExposureNot supplied

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

Exposure of B-lineage lymphoid cells to low energy electromagnetic fields stimulated Lyn and Syk protein tyrosine kinases, increased tyrosine phosphorylation of multiple substrates, and led to downstream activation of PKC. EMF-enhanced tyrosine phosphorylation occurred in Syk-deficient but not Lyn-deficient cells, and EMF stimulated Lyn activity in wild-type and Syk-deficient cells; PTK inhibitors (genistein or herbimycin A) abrogated the EMF-induced PKC signal.

Outcomes measured

Lyn kinase activity
Syk kinase activity
Protein tyrosine phosphorylation (multiple substrates)
Protein kinase C (PKC) activation
Effect of PTK inhibitors (genistein, herbimycin A) on EMF-induced PKC signal

Limitations

No EMF exposure parameters (frequency, field strength, SAR, duration) are provided in the abstract.
In vitro cell model; findings may not generalize to in vivo or human health outcomes.
Sample size and replication details are not reported in the abstract.
Outcomes are biochemical signaling endpoints; no direct clinical or disease endpoints are assessed.

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": null,
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "B-lineage lymphoid cells (including Lyn-deficient and Syk-deficient cells)",
  "sample_size": null,
  "outcomes": [
    "Lyn kinase activity",
    "Syk kinase activity",
    "Protein tyrosine phosphorylation (multiple substrates)",
    "Protein kinase C (PKC) activation",
    "Effect of PTK inhibitors (genistein, herbimycin A) on EMF-induced PKC signal"
  ],
  "main_findings": "Exposure of B-lineage lymphoid cells to low energy electromagnetic fields stimulated Lyn and Syk protein tyrosine kinases, increased tyrosine phosphorylation of multiple substrates, and led to downstream activation of PKC. EMF-enhanced tyrosine phosphorylation occurred in Syk-deficient but not Lyn-deficient cells, and EMF stimulated Lyn activity in wild-type and Syk-deficient cells; PTK inhibitors (genistein or herbimycin A) abrogated the EMF-induced PKC signal.",
  "effect_direction": "mixed",
  "limitations": [
    "No EMF exposure parameters (frequency, field strength, SAR, duration) are provided in the abstract.",
    "In vitro cell model; findings may not generalize to in vivo or human health outcomes.",
    "Sample size and replication details are not reported in the abstract.",
    "Outcomes are biochemical signaling endpoints; no direct clinical or disease endpoints are assessed."
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electromagnetic fields",
    "EMF",
    "B-lineage lymphoid cells",
    "Lyn kinase",
    "Syk kinase",
    "protein tyrosine phosphorylation",
    "protein kinase C",
    "PKC",
    "genistein",
    "herbimycin A",
    "signal transduction"
  ],
  "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: 10.1074/jbc.270.46.27666
PubMed: 7499232

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