Lili Wang1, Li He2, Guoqiang Bao3, Xin He4, Saijun Fan5, Haichao Wang6. 1. School of Radiation and Public Health, Soochow University Medical College, Suzhou, Jiangsu 215123, China. 2. Department of Ophthalmology, School of Medicine, Emory University, Atlanta, GA 30322, USA. 3. Department of General Surgery, Tangdu Hospital, The 4 Military Medical University, Xi'an, Shaanxi, 710032, China; Laboratory of Emergency Medicine, Feinstein Institute for Medical Research, Manhasset, NY 11030, USA. 4. Institute of Radiation Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300192, China. 5. School of Radiation and Public Health, Soochow University Medical College, Suzhou, Jiangsu 215123, China; Institute of Radiation Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300192, China. 6. School of Radiation and Public Health, Soochow University Medical College, Suzhou, Jiangsu 215123, China; Institute of Radiation Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300192, China; Laboratory of Emergency Medicine, Feinstein Institute for Medical Research, Manhasset, NY 11030, USA.
Abstract
OBJECTIVE: A nucleosomal protein, HMGB1, can be secreted by activated immune cells or passively released by dying cells, thereby amplifying rigorous inflammatory responses. In this study we aimed to test the possibility that ionizing radiation similarly induces cytoplasmic HMGB1 translocation and extracellular release. METHOD: Human skin fibroblast (GM0639) and bronchial epithelial (16HBE) cells and animals (rats) were exposed to X-ray radiation, and HMGB1 translocation and release were assessed by immunocytochemistry and immunoassay, respectively. RESULTS: At a wide dose range (4.0 - 12.0 Gy), X-ray radiation induced a dramatic cytoplasmic HMGB1 translocation, and triggered a time- and dose-dependent HMGB1 release both in vitro and in vivo. The radiation-mediated HMGB1 release was associated with noticeable chromosomal DNA damage and loss of cell viability. CONCLUSION: radiation induces HMGB1 cytoplasmic translocation and extracellular release through active secretion and passive leakage processes.
OBJECTIVE: A nucleosomal protein, HMGB1, can be secreted by activated immune cells or passively released by dying cells, thereby amplifying rigorous inflammatory responses. In this study we aimed to test the possibility that ionizing radiation similarly induces cytoplasmic HMGB1 translocation and extracellular release. METHOD:Human skin fibroblast (GM0639) and bronchial epithelial (16HBE) cells and animals (rats) were exposed to X-ray radiation, and HMGB1 translocation and release were assessed by immunocytochemistry and immunoassay, respectively. RESULTS: At a wide dose range (4.0 - 12.0 Gy), X-ray radiation induced a dramatic cytoplasmic HMGB1 translocation, and triggered a time- and dose-dependent HMGB1 release both in vitro and in vivo. The radiation-mediated HMGB1 release was associated with noticeable chromosomal DNA damage and loss of cell viability. CONCLUSION: radiation induces HMGB1 cytoplasmic translocation and extracellular release through active secretion and passive leakage processes.
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