Cytosolic calreticulin inhibits microwave radiation-induced microvascular endothelial cell injury through the integrin-focal adhesion kinase pathway.

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

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HarmLow evidencePaper 6560

Study snapshot

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

Study typein_vitro

Reported directionHarm

Evidence ratingLow

Abstract

OBJECTIVE: To determine the effects of cytosolic CRT on MR-induced MMEC injury, and the underlying mechanism. METHODS: MMECs were randomized into eight groups: control, AdCRT (infected with pAdCMV/V5-DEST-CRT adenovirus), stCRT (transfected with rCRT-siRNAs), Mock (transfected with scrambled siRNAs), MR (exposed to MR for six minutes), AdCRT + MR, stCRT + MR, and Mock + MR. The magnitude of cell injury were assessed by Annexin V-PI staining, LDH activity in culture medium, MMEC migration ability, ultrastructure and cytoskeletal stability. Subcellular colocalization of CRT and ConA or integrin were evaluated by immunocytochemistry. The mRNA and protein expression levels of target genes were examined by qRT-PCR and western blotting, respectively. RESULTS: MR-induced cytotoxicity was dose-dependent. Overexpression of cytosolic CRT suppressed MR injury, shown as decreased cell apoptosis, reduced LDH activity, enhanced cell migration capability, and maintenance of ultrastructure and cytoskeleton integrity. Conversely, CRT deficiency aggravated MR-induced injury. Exposure of AdCRT MMECs to MR promoted membrane translocation of CRT and the interaction of CRT-integrin-α. Correlation analysis revealed that integrin-α expression or FAK phosphorylation was positively associated with cytosolic CRT expression. CONCLUSIONS: Cytosolic CRT inhibits MR-induced MMEC injury through activation of the integrin-FAK pathway.

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 directionharm

PopulationNot supplied

Sample sizeNot supplied

Exposuresix minutes

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Microwave radiation (MR) induced dose-dependent cytotoxicity in mouse microvascular endothelial cells (MMECs). Overexpression of cytosolic calreticulin (CRT) reduced MR-associated injury markers (lower apoptosis and LDH activity) and improved migration and structural integrity, while CRT deficiency aggravated MR-induced injury. In AdCRT cells exposed to MR, CRT translocated to the membrane and interacted with integrin-α; integrin-α expression and FAK phosphorylation were positively associated with cytosolic CRT expression.

Outcomes measured

MMEC injury/cytotoxicity
apoptosis (Annexin V-PI)
LDH activity in culture medium
cell migration ability
ultrastructure
cytoskeletal stability
CRT membrane translocation
CRT-integrin-α interaction/colocalization
integrin-α expression
FAK phosphorylation

Limitations

In vitro cell model; findings may not generalize to in vivo or human exposures.
Exposure parameters beyond duration (e.g., frequency, SAR/power density) are not provided in the abstract.
Sample size and replication details are not reported in the abstract.

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": null,
    "source": "microwave radiation",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "six minutes"
  },
  "population": null,
  "sample_size": null,
  "outcomes": [
    "MMEC injury/cytotoxicity",
    "apoptosis (Annexin V-PI)",
    "LDH activity in culture medium",
    "cell migration ability",
    "ultrastructure",
    "cytoskeletal stability",
    "CRT membrane translocation",
    "CRT-integrin-α interaction/colocalization",
    "integrin-α expression",
    "FAK phosphorylation"
  ],
  "main_findings": "Microwave radiation (MR) induced dose-dependent cytotoxicity in mouse microvascular endothelial cells (MMECs). Overexpression of cytosolic calreticulin (CRT) reduced MR-associated injury markers (lower apoptosis and LDH activity) and improved migration and structural integrity, while CRT deficiency aggravated MR-induced injury. In AdCRT cells exposed to MR, CRT translocated to the membrane and interacted with integrin-α; integrin-α expression and FAK phosphorylation were positively associated with cytosolic CRT expression.",
  "effect_direction": "harm",
  "limitations": [
    "In vitro cell model; findings may not generalize to in vivo or human exposures.",
    "Exposure parameters beyond duration (e.g., frequency, SAR/power density) are not provided in the abstract.",
    "Sample size and replication details are not reported in the abstract."
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "microwave radiation",
    "microvascular endothelial cells",
    "calreticulin",
    "integrin",
    "focal adhesion kinase",
    "apoptosis",
    "LDH",
    "cell migration"
  ],
  "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/micc.12153
PubMed: 24930861

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