A longitudinal study of transcriptional profiling of carbon-ions exposure on the lung
10.3760/cma.j.cn113030-20200223-00070
- VernacularTitle:基于时间维度的全转录组水平重离子肺部放射效应研究
- Author:
Cheng ZHOU
1
;
Lei WEN
;
Shengfa SU
;
Shun LU
;
Zhiyuan XU
;
Hao CHENG
;
Changguo SHAN
;
Mingyao LAI
;
Linbo CAI
;
Longhua CHEN
;
Ming CHEN
;
Zhaoming ZHOU
Author Information
1. 南方医科大学南方医院放疗科，广州 510515
- Keywords:
Heavy ion;
Lung tissue injury;
Genome-wide transcriptional profiling;
Apoptosis;
Mouse
- From:
Chinese Journal of Radiation Oncology
2021;30(7):721-727
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression changes at the transcriptional level in normal lung tissues of mice after exposure to heavy ion radiation for different durations at different doses, aiming to provide evidence for exploring sensitive genes of heavy ion radiation, heavy ion radiation effect and the damage mechanism.Methods:Experiments on the temporal kinetics: the whole thorax of mice was irradiated with 14.5Gy carbon-ions and the total RNA of lung tissue was extracted at 3days, 7days, 3 weeks and 24 weeks. In dose-dependent experiment, the total RNA of lung tissue was extracted at 1 week after irradiated with a growing thoracic dose of 0, 7.5, 10.5, 12.5, 14.5, 17.5 and 20Gy. Protein-to-protein interaction (PPI) analysis and gene-ontology biological process enrichment analysis were performed on significant differentially expressed genes (DEGs).Results:A clearly differential expression patterns were observed at 3-day (acute stage), 1-week (subacute stage), 3-week (inflammatory stage) and 24-week (fibrosis stage) following 14.5Gy carbon-ions irradiation. Among those, the 3-day time point was found to be the mostly different from the other time points, whereas the 7-day time point had the highest uniformity with the other time points. Cellular apoptosis was the main type of cell death in normal lung tissues following carbon-ions exposure. The interactive genes of Phlda3, GDF15, Mgmt and Bax were identified as the radiosensitive genes, and Phlda3 was the center ( R=0.76, P<0.001). Conclusion:The findings in this study provide transcriptional insights into the biological mechanism underlying normal lung tissue toxicity induced by carbon-ions.
