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Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling 被引量:5

Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling
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摘要 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. 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.
出处 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2017年第5期323-332,共10页 生物医学与环境科学(英文版)
基金 supported by National Science Foundation of China(No.81172620)
关键词 Microwave Natural killer cells Cytotoxicity Apoptosis Cell cycle Perforin Microwave Natural killer cells Cytotoxicity Apoptosis Cell cycle Perforin
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