Microwave Radiation Injures Microvasculature Through Inducing Endoplasmic Reticulum Stress

Li, Yuzhen; Qu, Xiumei; Wang, Xiao-Reng; Liu, Mi; Wang, Chen; Lv, Zhen-Rong; Li, Weihong; Tao, Tianqi; Song, Dandan; Li, Xiuhua

doi:10.1111/micc.12122

Cited by 6 publications

(2 citation statements)

References 21 publications

(27 reference statements)

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“…The indicators of endoplasmic reticulum stress used in studies of microwave radiation bioeffects mainly included the transcription factors XBP1, ATF4 and CHOP [ 224 , 249 ]. A recent study showed that microwave radiation at frequencies between 900 MHz and 2450 MHz could decrease the expression of XBP1 splicing mRNA and increase the expression of ATF4 and CHOP mRNA in rat brains, suggesting the activation of endoplasmic reticulum stress [ 224 ].…”

Section: Indicators Of Microwave Radiation-induced Biological Injuriementioning

confidence: 99%

Establishment of injury models in studies of biological effects induced by microwave radiation

2021

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Microwave radiation has been widely used in various fields, such as communication, industry, medical treatment, and military applications. Microwave radiation may cause injuries to both the structures and functions of various organs, such as the brain, heart, reproductive organs, and endocrine organs, which endanger human health. Therefore, it is both theoretically and clinically important to conduct studies on the biological effects induced by microwave radiation. The successful establishment of injury models is of great importance to the reliability and reproducibility of these studies. In this article, we review the microwave exposure conditions, subjects used to establish injury models, the methods used for the assessment of the injuries, and the indicators implemented to evaluate the success of injury model establishment in studies on biological effects induced by microwave radiation.

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Section: Indicators Of Microwave Radiation-induced Biological Injuriementioning

confidence: 99%

Establishment of injury models in studies of biological effects induced by microwave radiation

2021

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“…In vivo studies suggested that EMR triggered cell apoptosis by regulating the caspase-3 signaling pathway [ 9 , 10 ] and Bcl-2 and bax gene expression [ 11 ]. Li Y et al [ 12 ] found that apoptosis could be induced by increasing endoplasmic reticulum stress after exposure. RF-EMR depressed cell proliferation [ 13 , 14 ] and lead cell cycle arrest, with an increased proportion of cells at the S phase [ 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanism of Malignant Transformation of Balb/c-3T3 Cells Induced by Long-Term Exposure to 1800 MHz Radiofrequency Electromagnetic Radiation (RF-EMR)

Ding

Xiang

et al. 2022

Bioengineering

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Purpose: We aimed to investigate RF-EMR-induced cell malignant transformation. Methods: We divided Balb/c-3T3 cells into sham and expo groups. The expo groups were exposed to a 1800 MHz RF continuous wave for 40 and 60 days, for 4 h per day. The sham group was sham-exposed. Cells were harvested for a cell transformation assay, transplantation in severe combined immune deficient (SCID) mice, soft agar clone formation detection, and a transwell assay. The mRNA microarray assay was used to declare key genes and pathways. Results: The exposed Balb/c-3T3 cells showed a strong increase in cell proliferation and migration. Malignant transformation was observed in expo Balb/c-3T3 cells exposed for 40 days and 60 days, which was symbolized with visible foci and clone formation. Expo Balb/c-3T3 cells that were exposed for 40 days and 60 days produced visible tumors in the SCID mice. Lipid metabolism was the key biological process and pathway involved. The mevalonate (MVA) pathway was the key metabolic pathway. The interacted miRNAs could be further research targets to examine the molecular mechanism of the carcinogenic effects of long-term exposure. Conclusion: Exposure for 40 and 60 days to 1800 MHz RF-EMR induced malignant transformation in Balb/c-3T3 cells at the SAR of 8.0 W/kg. We declared that lipid metabolism was the pivotal biological process and pathway. The MVA pathway was the key metabolic pathway.

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Calreticulin attenuated microwave radiation-induced human microvascular endothelial cell injury through promoting actin acetylation and polymerization

Wang

Tao

et al. 2017

Cell Stress and Chaperones

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Recent work reveals that actin acetylation modification has been linked to different normal and disease processes and the effects associated with metabolic and environmental stressors. Herein, we highlight the effects of calreticulin on actin acetylation and cell injury induced by microwave radiation in human microvascular endothelial cell (HMEC). HMEC injury was induced by high-power microwave of different power density (10, 30, 60, 100 mW/cm, for 6 min) with or without exogenous recombinant calreticulin. The cell injury was assessed by lactate dehydrogenase (LDH) activity and Cell Counting Kit-8 in culture medium, migration ability, intercellular junction, and cytoskeleton staining in HMEC. Western blotting analysis was used to detected calreticulin expression in cytosol and nucleus and acetylation of globular actin (G-actin). We found that HMEC injury was induced by microwave radiation in a dose-dependent manner. Pretreatment HMEC with calreticulin suppressed microwave radiation-induced LDH leakage and increased cell viability and improved microwave radiation-induced decrease in migration, intercellular junction, and cytoskeleton. Meanwhile, pretreatment HMEC with exogenous calreticulin upregulated the histone acetyltransferase activity and the acetylation level of G-actin and increased the fibrous actin (F-actin)/G-actin ratio. We conclude that exogenous calreticulin protects HMEC against microwave radiation-induced injury through promoting actin acetylation and polymerization.

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Microwave Radiation Injures Microvasculature Through Inducing Endoplasmic Reticulum Stress

Abstract: Microwave radiation induces microvascular injury by triggering the apoptotic pathway of endoplasmic reticulum stress. This article is protected by copyright. All rights reserved.

Cited by 6 publications

References 21 publications

Establishment of injury models in studies of biological effects induced by microwave radiation

Establishment of injury models in studies of biological effects induced by microwave radiation

Molecular Mechanism of Malignant Transformation of Balb/c-3T3 Cells Induced by Long-Term Exposure to 1800 MHz Radiofrequency Electromagnetic Radiation (RF-EMR)

Calreticulin attenuated microwave radiation-induced human microvascular endothelial cell injury through promoting actin acetylation and polymerization

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