Liu Fang, Wang Zhuanzi, Li Wenjian, Wei Yanting
Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, 730000, China; University of Chinese Academy of Sciences, Beijing, 100049, China.
Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, 730000, China.
Mutat Res Genet Toxicol Environ Mutagen. 2019 Mar;839:49-58. doi: 10.1016/j.mrgentox.2019.01.014. Epub 2019 Jan 26.
The need to understand the health effects of heavy ion irradiation is motivated by the use of this modality in radiotherapy and by the potential for exposure during space missions. We have studied the effects of carbon-ion total-body irradiation on the hematopoietic system of the mouse and, in particular, the transcriptional response of bone marrow (BM) cells. Carbon-ion irradiation caused BM cell DNA damage, apoptosis, elevated ROS, and myelosuppression. Transcriptomic analysis showed that overall gene expression in irradiated BM cells differed significantly from the controls. Of 253 genes that were modulated, 192 were up-regulated and 61 down-regulated. Gene ontology analysis showed that the modulated genes are involved in DNA damage response signaling, DNA repair, apoptosis, and the immune response. Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that these functions are regulated by the p38 MAPK, TNF, and apoptosis pathways. These findings indicate pathways that may be involved in protection against carbon ion radiation injury.
了解重离子辐射对健康的影响，这一需求源于这种治疗方式在放射治疗中的应用以及太空任务期间可能存在的暴露风险。我们研究了碳离子全身照射对小鼠造血系统的影响，特别是对骨髓（BM）细胞的转录反应。碳离子照射导致BM细胞DNA损伤、凋亡、活性氧升高以及骨髓抑制。转录组分析表明，照射后BM细胞中的整体基因表达与对照组有显著差异。在253个被调节的基因中，192个上调，61个下调。基因本体分析表明，被调节的基因参与DNA损伤反应信号传导、DNA修复、凋亡和免疫反应。京都基因与基因组百科全书通路分析表明，这些功能受p38丝裂原活化蛋白激酶、肿瘤坏死因子和凋亡通路调节。这些发现表明了可能参与抵御碳离子辐射损伤的途径。
