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
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.
Biomed Environ Sci. 2017 May;30(5):323-332. doi: 10.3967/bes2017.043.
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.
研究微波诱导的自然杀伤（NK）细胞形态和功能损伤并揭示其机制。
将NK-92细胞暴露于10、30和50 mW/cm²的微波下5分钟。在暴露后1小时和24小时检测超微结构变化、细胞凋亡和细胞周期调控。在暴露后1小时测定细胞毒性活性，同时在暴露后1小时、6小时和12小时检测穿孔素和NKG2D表达。为阐明机制，在暴露后1小时检测磷酸化ERK（p-ERK）。此外，使用U0126阻断ERK信号后，分析微波诱导的细胞凋亡和细胞周期调控。
微波暴露后1小时检测到微波诱导的形态和超微结构损伤、剂量依赖性凋亡（P < 0.001）和细胞周期阻滞（P < 0.001）。此外，在50 mW/cm²微波暴露后24小时仍检测到明显凋亡（P < 0.01）。在30 mW/cm²微波暴露模型中，微波在暴露后1小时损害NK-92细胞的细胞毒性活性，并在暴露后1小时和6小时下调穿孔素蛋白（P < 0.05）。此外，暴露后1小时p-ERK下调（P < 0.05），而ERK阻断显著促进微波诱导的凋亡（P < 0.05）和穿孔素下调（P < 0.01）。
微波剂量依赖性地诱导NK-92细胞的形态和功能损伤，可能通过ERK介导的凋亡和穿孔素表达调控。
