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 |
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Abstract | 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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AbstractList | To investigate microwave-induced morphological and functional injury of natural killer (NK) cells and uncover their mechanisms.
NK-92 cells were exposed to 10, 30, and 50 mW/cm2 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 NKG2D 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.
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 mW/cm2 microwave exposure (P < 0.01). In the 30 mW/cm2 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).
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. To investigate microwave-induced morphological and functional injury of natural killer (NK) cells and uncover their mechanisms.OBJECTIVETo investigate microwave-induced morphological and functional injury of natural killer (NK) cells and uncover their mechanisms.NK-92 cells were exposed to 10, 30, and 50 mW/cm2 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 NKG2D 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.METHODSNK-92 cells were exposed to 10, 30, and 50 mW/cm2 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 NKG2D 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.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 mW/cm2 microwave exposure (P < 0.01). In the 30 mW/cm2 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).RESULTSMicrowave-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 mW/cm2 microwave exposure (P < 0.01). In the 30 mW/cm2 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).Microwave dose-dependently induced morphological and functional injury in NK-92 cells, possibly through ERK-mediated regulation of apoptosis and perforin expression.CONCLUSIONMicrowave 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 mW/cm2 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 NKG2D 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 mW/cm2 microwave exposure (P < 0.01). In the 30 mW/cm2 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. |
Author | 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 |
AuthorAffiliation | 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 |
AuthorAffiliation_xml | – name: 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 |
Author_xml | – sequence: 1 givenname: Li surname: ZHAO fullname: ZHAO, Li organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China – sequence: 2 givenname: Jing surname: LI fullname: LI, Jing organization: Department of Pathology, General Hospital of Beijing Command of PLA, Beijing 100700, China – sequence: 3 givenname: Yan Hui surname: HAO fullname: HAO, Yan Hui organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China – sequence: 4 givenname: Ya Bing surname: GAO fullname: GAO, Ya Bing organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China – sequence: 5 givenname: Shui Ming surname: WANG fullname: WANG, Shui Ming organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China – sequence: 6 givenname: Jing surname: ZHANG fullname: ZHANG, Jing organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China – sequence: 7 givenname: Ji surname: DONG fullname: DONG, Ji organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China – sequence: 8 givenname: Hong Mei surname: ZHOU fullname: ZHOU, Hong Mei organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China – sequence: 9 givenname: Shu Chen surname: LIU fullname: LIU, Shu Chen email: liusc118@163.com organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China – sequence: 10 givenname: Rui Yun surname: PENG fullname: PENG, Rui Yun email: ruiyunpeng18@126.com organization: Department of Experimental Pathology, Beijing Institute of Radiation Medicine, Beijing 100850, China |
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Copyright | 2017 The Editorial Board of Biomedical and Environmental Sciences Copyright © 2017 The Editorial Board of Biomedical and Environmental Sciences. Published by China CDC. All rights reserved. Copyright © Wanfang Data Co. Ltd. All Rights Reserved. |
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Keywords | Microwave Cytotoxicity Natural killer cells Perforin Cell cycle Apoptosis |
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Notes | 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 |
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Snippet | Objective To investigate microwave-induced morphological and functional injury of natural killer(NK) cells and uncover their mechanisms. Methods NK-92 cells... To investigate microwave-induced morphological and functional injury of natural killer (NK) cells and uncover their mechanisms. NK-92 cells were exposed to 10,... To investigate microwave-induced morphological and functional injury of natural killer (NK) cells and uncover their mechanisms.OBJECTIVETo investigate... Objective To investigate microwave-induced morphological and functional injury of natural killer (NK)cells and uncover their mechanisms.Methods NK-92 cells... |
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SubjectTerms | Apoptosis Apoptosis - radiation effects Cell cycle Cell Cycle - radiation effects Cell Line Cytotoxicity Dose-Response Relationship, Radiation Down-Regulation Humans Killer Cells, Natural - radiation effects MAP Kinase Signaling System Microwave Microwaves - adverse effects Natural killer cells NK Cell Lectin-Like Receptor Subfamily K - genetics NK Cell Lectin-Like Receptor Subfamily K - metabolism Perforin Signal Transduction |
Title | Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling |
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