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 in | Biomedical and environmental sciences Vol. 30; no. 5; pp. 323 - 332 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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 |
Subjects | |
Online Access | Get full text |
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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. |
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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 |