Microwave Radiation Injures Microvasculature Through Inducing Endoplasmic Reticulum Stress
maandag, 31 augustus 2015 - Categorie: Onderzoeken
Li Y, Qu X, Wang X, Liu M, Wang C, Lv Z, Li W, Tao T, Song D, Liu X. Microwave radiation injures microvasculature through inducing endoplasmic reticulum stress. Microcirculation 21: 490–498, 2014.
1Department of Pathophysiology, Chinese PLA General Hospital, Beijing, China
2State Key Laboratory of Kidney Disease, Chinese PLA General Hospital, Beijing, China
3Outpatient Department, Fourth Military Medical University, Xi'an, China
microwave radiation;microvasculature;microvascular endothelial cell;apotosis;endoplasmic reticulum stress
The study aimed to investigate the effect of microwave radiation on microvasculature as well as the underlying mechanisms.
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.
Microwave radiation decreased microvascular diameters and blood perfusion, and 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.
Microwave radiation induces microvascular injury by triggering the apoptotic pathway of endoplasmic reticulum stress.
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