Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling

Objective To investigate microwave-induced morphological and functional injury of natural killer(NK) cells and uncover their mechanisms. Methods NK-92 cells were exposed to 10, 30, and 50 m W/cm~2 microwaves for 5 min. Ultrastructural changes, cellular apoptosis and cell cycle regulation were detect...

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Published inBiomedical and environmental sciences Vol. 30; no. 5; pp. 323 - 332
Main Authors ZHAO, Li, LI, Jing, HAO, Yan Hui, GAO, Ya Bing, WANG, Shui Ming, ZHANG, Jing, DONG, Ji, ZHOU, Hong Mei, LIU, Shu Chen, PENG, Rui Yun
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.05.2017
Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China%Department of Pathology, General Hospital of Beijing Command of PLA, Beijing 100700, China
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Summary:Objective To investigate microwave-induced morphological and functional injury of natural killer(NK) cells and uncover their mechanisms. Methods NK-92 cells were exposed to 10, 30, and 50 m W/cm~2 microwaves for 5 min. Ultrastructural changes, cellular apoptosis and cell cycle regulation were detected at 1 h and 24 h after exposure. Cytotoxic activity was assayed at 1 h after exposure, while perforin and NKG2 D expression were detected at 1 h, 6 h, and 12 h after exposure. To clarify the mechanisms, phosphorylated ERK(p-ERK) was detected at 1 h after exposure. Moreover, microwave-induced cellular apoptosis and cell cycle regulation were analyzed after blockade of ERK signaling by using U0126. Results Microwave-induced morphological and ultrastructural injury, dose-dependent apoptosis(P 〈 0.001) and cell cycle arrest(P 〈 0.001) were detected at 1 h after microwave exposure. Moreover, significant apoptosis was still detected at 24 h after 50 m W/cm~2 microwave exposure(P 〈 0.01). In the 30 m W/cm~2 microwave exposure model, microwaves impaired the cytotoxic activity of NK-92 cells at 1 h and down regulated perforin protein both at 1 h and 6 h after exposure(P 〈 0.05). Furthermore, p-ERK was down regulated at 1 h after exposure(P 〈 0.05), while ERK blockade significantly promoted microwave-induced apoptosis(P 〈 0.05) and downregulation of perforin(P 〈 0.01). Conclusion Microwave dose-dependently induced morphological and functional injury in NK-92 cells, possibly through ERK-mediated regulation of apoptosis and perforin expression.
Bibliography:Objective To investigate microwave-induced morphological and functional injury of natural killer(NK) cells and uncover their mechanisms. Methods NK-92 cells were exposed to 10, 30, and 50 m W/cm~2 microwaves for 5 min. Ultrastructural changes, cellular apoptosis and cell cycle regulation were detected at 1 h and 24 h after exposure. Cytotoxic activity was assayed at 1 h after exposure, while perforin and NKG2 D expression were detected at 1 h, 6 h, and 12 h after exposure. To clarify the mechanisms, phosphorylated ERK(p-ERK) was detected at 1 h after exposure. Moreover, microwave-induced cellular apoptosis and cell cycle regulation were analyzed after blockade of ERK signaling by using U0126. Results Microwave-induced morphological and ultrastructural injury, dose-dependent apoptosis(P 〈 0.001) and cell cycle arrest(P 〈 0.001) were detected at 1 h after microwave exposure. Moreover, significant apoptosis was still detected at 24 h after 50 m W/cm~2 microwave exposure(P 〈 0.01). In the 30 m W/cm~2 microwave exposure model, microwaves impaired the cytotoxic activity of NK-92 cells at 1 h and down regulated perforin protein both at 1 h and 6 h after exposure(P 〈 0.05). Furthermore, p-ERK was down regulated at 1 h after exposure(P 〈 0.05), while ERK blockade significantly promoted microwave-induced apoptosis(P 〈 0.05) and downregulation of perforin(P 〈 0.01). Conclusion Microwave dose-dependently induced morphological and functional injury in NK-92 cells, possibly through ERK-mediated regulation of apoptosis and perforin expression.
11-2816/Q
Microwave Natural killer cells Cytotoxicity Apoptosis Cell cycle Perforin
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0895-3988
2214-0190
DOI:10.3967/bes2017.043