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Journal Article

Citation

Li Y, Qu X, Wang X, Liu M, Wang C, Lv Z, Li W, Tao T, Song D, Liu X. Microcirculation 2014; ePub(ePub): ePub.

Affiliation

Department of Pathophysiology, Chinese PLA General Hospital, 100853, Beijing; State Key Laboratory of Kidney Disease, Chinese PLA General Hospital, 100853, Beijing.

Copyright

(Copyright © 2014)

DOI

10.1111/micc.12122

PMID

24635541

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.


Language: en

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