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Transcriptional response of murine bone marrow cells to total-body carbon-ion irradiation.
Mutation Research/Genetic Toxicology and Environmental Mutagenesis ( IF 1.9 ) Pub Date : 2019-02-13 , DOI: 10.1016/j.mrgentox.2019.01.014
Fang Liu 1 , Zhuanzi Wang 2 , Wenjian Li 2 , Yanting Wei 3
Affiliation  

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.

中文翻译:

鼠骨髓细胞对全身碳离子辐射的转录反应。

理解重离子辐射对健康的影响的动机是由于这种方式在放射治疗中的应用以及太空飞行期间可能暴露于其中。我们已经研究了碳离子全身照射对小鼠造血系统的影响,尤其是骨髓(BM)细胞的转录反应。碳离子辐照引起BM细胞DNA损伤,凋亡,ROS升高和骨髓抑制。转录组学分析表明,照射的BM细胞中的总体基因表达与对照显着不同。在253个受调节的基因中,有192个被上调,而61个被下调。基因本体分析表明,调节后的基因参与了DNA损伤应答信号,DNA修复,细胞凋亡和免疫应答。京都基因与基因组百科全书通路分析表明,这些功能受p38 MAPK,TNF和凋亡通路的调节。这些发现表明可能参与了防止碳离子辐射损伤的途径。
更新日期:2019-11-01
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