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Calreticulin protects rat microvascular endothelial cells against microwave radiation-induced injury by attenuating endoplasmic reticulum stress.

PAPER pubmed Microcirculation (New York, N.Y. : 1994) 2014 In vitro study Effect: harm Evidence: Low

Abstract

OBJECTIVE: This study was designed to evaluate whether exogenous CRT was beneficial for alleviating MR-induced injury by suppressing ER stress in rat MMECs. METHODS: MMECs were pretreated with CRT (25 pg/mL) for 12 hours, followed by the exposure to 2.856 GHz radiation at a mean power density of 30 mW/cm(2) for six minutes. MR-induced injury in MMECs was evaluated by LDH leakage, apoptosis, and cell viability analysis. The expression of GRP78, CRT, CHOP, Bcl-2, and Bax were examined by Western blot analysis to reflect ER stress response and ER stress-related apoptosis. RESULTS: MR induced marked MMECs injury, as shown by increased LDH leakage and apoptosis rate and decreased cell viability. MR also induced excessive ER stress, characterized by increased expression of GRP78 and CRT, and ER stress-related apoptotic signaling as well, as shown by the upregulation of CHOP and Bax and the downregulation of Bcl-2. Exogenous CRT pretreatment remarkably attenuated MR-induced cell apoptosis and LDH leakage, ER stress, and activation of the ER stress-related apoptotic signaling. CONCLUSIONS: Exogenous CRT attenuates MR-induced ER stress-related apoptosis by suppressing CHOP-mediated apoptotic signaling pathways in MMECs.

AI evidence extraction

At a glance
Study type
In vitro study
Effect direction
harm
Population
Rat microvascular endothelial cells (MMECs)
Sample size
Exposure
microwave · 2856 MHz · 6 minutes (after 12 h pretreatment with CRT)
Evidence strength
Low
Confidence: 78% · Peer-reviewed: yes

Main findings

Exposure to 2.856 GHz radiation (30 mW/cm^2 for 6 minutes) induced injury in rat MMECs, with increased LDH leakage and apoptosis and decreased cell viability, alongside increased GRP78/CRT and pro-apoptotic signaling (increased CHOP and Bax, decreased Bcl-2). Pretreatment with exogenous CRT (25 pg/mL for 12 hours) attenuated MR-induced apoptosis, LDH leakage, ER stress markers, and ER stress-related apoptotic signaling.

Outcomes measured

  • LDH leakage
  • Apoptosis rate
  • Cell viability
  • Protein expression: GRP78
  • Protein expression: calreticulin (CRT)
  • Protein expression: CHOP
  • Protein expression: Bcl-2
  • Protein expression: Bax
  • Endoplasmic reticulum (ER) stress response
  • ER stress-related apoptotic signaling

Limitations

  • In vitro cell model; findings may not generalize to whole organisms or humans
  • Sample size not reported in abstract
  • Exposure metric reported as mean power density; SAR not provided

Suggested hubs

  • mechanisms-er-stress (0.9)
    Study focuses on ER stress markers (GRP78, CHOP) and ER stress-mediated apoptosis after microwave exposure.
View raw extracted JSON
{
    "study_type": "in_vitro",
    "exposure": {
        "band": "microwave",
        "source": null,
        "frequency_mhz": 2856,
        "sar_wkg": null,
        "duration": "6 minutes (after 12 h pretreatment with CRT)"
    },
    "population": "Rat microvascular endothelial cells (MMECs)",
    "sample_size": null,
    "outcomes": [
        "LDH leakage",
        "Apoptosis rate",
        "Cell viability",
        "Protein expression: GRP78",
        "Protein expression: calreticulin (CRT)",
        "Protein expression: CHOP",
        "Protein expression: Bcl-2",
        "Protein expression: Bax",
        "Endoplasmic reticulum (ER) stress response",
        "ER stress-related apoptotic signaling"
    ],
    "main_findings": "Exposure to 2.856 GHz radiation (30 mW/cm^2 for 6 minutes) induced injury in rat MMECs, with increased LDH leakage and apoptosis and decreased cell viability, alongside increased GRP78/CRT and pro-apoptotic signaling (increased CHOP and Bax, decreased Bcl-2). Pretreatment with exogenous CRT (25 pg/mL for 12 hours) attenuated MR-induced apoptosis, LDH leakage, ER stress markers, and ER stress-related apoptotic signaling.",
    "effect_direction": "harm",
    "limitations": [
        "In vitro cell model; findings may not generalize to whole organisms or humans",
        "Sample size not reported in abstract",
        "Exposure metric reported as mean power density; SAR not provided"
    ],
    "evidence_strength": "low",
    "confidence": 0.7800000000000000266453525910037569701671600341796875,
    "peer_reviewed_likely": "yes",
    "keywords": [
        "calreticulin",
        "CRT",
        "microwave radiation",
        "2.856 GHz",
        "microvascular endothelial cells",
        "MMECs",
        "endoplasmic reticulum stress",
        "GRP78",
        "CHOP",
        "Bcl-2",
        "Bax",
        "apoptosis",
        "LDH leakage"
    ],
    "suggested_hubs": [
        {
            "slug": "mechanisms-er-stress",
            "weight": 0.90000000000000002220446049250313080847263336181640625,
            "reason": "Study focuses on ER stress markers (GRP78, CHOP) and ER stress-mediated apoptosis after microwave exposure."
        }
    ]
}

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AI-extracted fields are generated from the abstract/metadata and may be incomplete or incorrect. This content is for informational purposes only and is not medical advice.

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