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

Microcirculation (New York, N.Y. : 1994) · 2014 · Harm · Low evidence

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HarmLow evidencePaper 6564

Study snapshot

PublicationMicrocirculation (New York, N.Y. : 1994) · 2014

Study typein_vitro

Reported directionHarm

Evidence ratingLow

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.

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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 directionharm

PopulationRat microvascular endothelial cells (MMECs)

Sample sizeNot supplied

Exposuremicrowave · 2856 MHz · 6 minutes (after 12 h pretreatment with CRT)

Evidence strengthLowConfidence: 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

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": 0.78,
  "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": 0.9,
      "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 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/micc.12126
PubMed: 24589181

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