Microwave radiation injuries microvasculature through inducing endoplasmic reticulum stress.

Abstract

OBJECTIVE: The study aimed to investigate the effect of microwave radiation on microvasculature as well as the underlying mechanisms. METHODS: Sprague Dawley rats were exposed to microwave radiation. Microvascular diameters, flow velocity, blood perfusion and permeability were measured. Cultured endothelial cells from microvessels were subjected to microwave radiation. Cytoskeleton, apoptosis, protein synthesis and the markers of endoplasmic reticulum stress including 78-kDa glucose-regulated protein and calreticulin in endothelial cells were examined. RESULTS: Microwave radiation decreased microvascular diameters and blood perfusion, increased the permeability of microvessles. And microwave radiation induced the formation of stress fibers, apoptosis, and LDH leakage from microvascular endothelial cells. Also, when microvascular endothelial cells were exposed to microwaves, protein synthesis was significantly elevated. We found that upon microwave radiation, the expression of 78-kDa glucose-regulated protein and calreticulin were greatly upregulated in microvascular endothelial cells. We also investigated possible signaling pathways for endoplasmic reticulum stress-initiated apoptosis. C/EBP homologous protein (CHOP) pathway was activated in microvascular endothelial cells exposed to microwaves. CONCLUSIONS: Microwave radiation induces microvascular injury by triggering the apoptotic pathway of endoplasmic reticulum stress. This article is protected by copyright. All rights reserved.

AI evidence extraction

Main findings

In rats, microwave radiation decreased microvascular diameters and blood perfusion and increased microvessel permeability. In cultured microvascular endothelial cells, microwave exposure induced stress fiber formation, apoptosis, and LDH leakage, increased protein synthesis, upregulated ER-stress markers (GRP78 and calreticulin), and activated the CHOP pathway.

Outcomes measured

• Microvascular diameter
• Microvascular flow velocity
• Blood perfusion
• Microvascular permeability
• Endothelial cell cytoskeleton (stress fibers)
• Endothelial cell apoptosis
• LDH leakage
• Protein synthesis
• Endoplasmic reticulum stress markers (78-kDa glucose-regulated protein/GRP78, calreticulin)
• CHOP pathway activation

Limitations

• No exposure parameters reported (e.g., frequency, SAR, duration).
• Sample size not reported in abstract.
• Unclear whether sham controls, blinding, or randomization were used (not stated).

Suggested hubs

• mechanisms-er-stress (0.86)
  Study focuses on ER stress markers (GRP78, calreticulin) and CHOP-mediated apoptosis after microwave exposure.
• animal-studies (0.75)
  Includes in vivo rat exposure outcomes on microvasculature.

{
    "study_type": "animal",
    "exposure": {
        "band": "microwave",
        "source": null,
        "frequency_mhz": null,
        "sar_wkg": null,
        "duration": null
    },
    "population": "Sprague Dawley rats; cultured microvascular endothelial cells",
    "sample_size": null,
    "outcomes": [
        "Microvascular diameter",
        "Microvascular flow velocity",
        "Blood perfusion",
        "Microvascular permeability",
        "Endothelial cell cytoskeleton (stress fibers)",
        "Endothelial cell apoptosis",
        "LDH leakage",
        "Protein synthesis",
        "Endoplasmic reticulum stress markers (78-kDa glucose-regulated protein/GRP78, calreticulin)",
        "CHOP pathway activation"
    ],
    "main_findings": "In rats, microwave radiation decreased microvascular diameters and blood perfusion and increased microvessel permeability. In cultured microvascular endothelial cells, microwave exposure induced stress fiber formation, apoptosis, and LDH leakage, increased protein synthesis, upregulated ER-stress markers (GRP78 and calreticulin), and activated the CHOP pathway.",
    "effect_direction": "harm",
    "limitations": [
        "No exposure parameters reported (e.g., frequency, SAR, duration).",
        "Sample size not reported in abstract.",
        "Unclear whether sham controls, blinding, or randomization were used (not stated)."
    ],
    "evidence_strength": "low",
    "confidence": 0.7800000000000000266453525910037569701671600341796875,
    "peer_reviewed_likely": "yes",
    "keywords": [
        "microwave radiation",
        "microvasculature",
        "endothelial cells",
        "permeability",
        "blood perfusion",
        "apoptosis",
        "endoplasmic reticulum stress",
        "GRP78",
        "calreticulin",
        "CHOP"
    ],
    "suggested_hubs": [
        {
            "slug": "mechanisms-er-stress",
            "weight": 0.85999999999999998667732370449812151491641998291015625,
            "reason": "Study focuses on ER stress markers (GRP78, calreticulin) and CHOP-mediated apoptosis after microwave exposure."
        },
        {
            "slug": "animal-studies",
            "weight": 0.75,
            "reason": "Includes in vivo rat exposure outcomes on microvasculature."
        }
    ]
}

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