Ionizing Radiation Induces HMGB1 Cytoplasmic Translocation and Extracellular Release.

Guo ji fang she yi xue he yi xue za zhi = International journal of radiation medicine and nuclear medicine Pub Date : 2016-03-01 Epub Date: 2016-04-15

Lili Wang, Li He, Guoqiang Bao, Xin He, Saijun Fan, Haichao Wang

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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.

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电离辐射诱导HMGB1胞质易位和胞外释放。

目的:核小体蛋白HMGB1可由活化的免疫细胞分泌或由死亡细胞被动释放，从而放大剧烈的炎症反应。在这项研究中，我们旨在测试电离辐射类似地诱导细胞质HMGB1易位和细胞外释放的可能性。方法:x线照射人皮肤成纤维细胞(GM0639)、支气管上皮细胞(16HBE)和动物(大鼠)，分别用免疫细胞化学和免疫测定法测定HMGB1的易位和释放。结果:在大剂量范围内(4.0 ~ 12.0 Gy)， x射线辐射可诱导HMGB1在细胞质中发生剧烈的易位，并引发HMGB1在体外和体内的时间和剂量依赖性释放。辐射介导的HMGB1释放与明显的染色体DNA损伤和细胞活力丧失有关。结论:辐射可通过主动分泌和被动渗漏两种途径诱导HMGB1胞质易位和胞外释放。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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