Abstract：
OBJECTIVE: The cardiovascular system effects of environmental low-dose radiation exposure on radiation practitioners remain uncertain and require further investigation. The aim of this study was to initially investigate and explore the mechanisms by which low-dose radiation may contribute to atherosclerosis through a multi-omics joint comprehensive basic experiment.
METHODS: We used WGCNA and differential analyses to identify shared genes and potential pathways between radiation injury and atherosclerosis sequencing datasets, as well as tissue transcriptome immune infiltration level extrapolation and single-cell transcriptome data correction using the CIBERSORT deconvolution algorithm. Animal models were constructed by combining a high-fat diet with 5 Gy γ-ray whole-body low-dose ionizing radiation. The detection of NETs release was validated by enzyme-linked immunosorbent assay.
RESULTS: Analysis reveals shared genes in both datasets of post-irradiation and atherosclerosis, suggesting that immune system neutrophils may be a key node connecting radiation to atherosclerosis. NETs released by neutrophil death can influence the development of atherosclerosis. Animal experiments showed that the number of neutrophils decreased (P < 0.05) and the concentration of NETs reduced after low-dose radiation compared with the control group, and the concentration of NETs significantly increased (P < 0.05) in the HF group. Endothelial plaques were significantly increased in the high-fat feed group and significantly decreased in the low-dose radiation group compared with the control group.
CONCLUSIONS: Long-term low-dose ionizing radiation exposure stimulates neutrophils and inhibits their production of NETs, resulting in inhibition of atherosclerosis.
METHODS: We used WGCNA and differential analyses to identify shared genes and potential pathways between radiation injury and atherosclerosis sequencing datasets, as well as tissue transcriptome immune infiltration level extrapolation and single-cell transcriptome data correction using the CIBERSORT deconvolution algorithm. Animal models were constructed by combining a high-fat diet with 5 Gy γ-ray whole-body low-dose ionizing radiation. The detection of NETs release was validated by enzyme-linked immunosorbent assay.
RESULTS: Analysis reveals shared genes in both datasets of post-irradiation and atherosclerosis, suggesting that immune system neutrophils may be a key node connecting radiation to atherosclerosis. NETs released by neutrophil death can influence the development of atherosclerosis. Animal experiments showed that the number of neutrophils decreased (P < 0.05) and the concentration of NETs reduced after low-dose radiation compared with the control group, and the concentration of NETs significantly increased (P < 0.05) in the HF group. Endothelial plaques were significantly increased in the high-fat feed group and significantly decreased in the low-dose radiation group compared with the control group.
CONCLUSIONS: Long-term low-dose ionizing radiation exposure stimulates neutrophils and inhibits their production of NETs, resulting in inhibition of atherosclerosis.
摘要：
目的：环境低剂量辐射对放射从业人员的心血管系统影响仍不确定，需要进一步研究。本研究的目的是通过多组学联合综合基础实验，初步探讨低剂量辐射可能导致动脉粥样硬化的机制。
方法：我们使用WGCNA和差异分析来鉴定辐射损伤和动脉粥样硬化测序数据集之间的共有基因和潜在通路，以及使用CIBERSORT反卷积算法进行组织转录组免疫浸润水平外推和单细胞转录组数据校正。通过将高脂饮食与5Gyγ射线全身低剂量电离辐射相结合来构建动物模型。通过酶联免疫吸附试验验证了NETs释放的检测。
结果：分析揭示了辐射后和动脉粥样硬化两个数据集中的共有基因，提示免疫系统中性粒细胞可能是连接辐射和动脉粥样硬化的关键节点。NETs释放的中性粒细胞逝世亡能够影响动脉粥样硬化的发展。动物实验表明,低剂量辐射后中性粒细胞数量减少(P<0.05),NETs浓度降低,HF组NETs浓度显著升高(P<0.05)。与对照组相比，高脂饲料组血管内皮斑块明显增多，低剂量辐射组血管内皮斑块明显减少。
结论：长期低剂量电离辐射照射刺激嗜中性粒细胞并抑制其产生NETs，导致动脉粥样硬化的抑制。
方法：我们使用WGCNA和差异分析来鉴定辐射损伤和动脉粥样硬化测序数据集之间的共有基因和潜在通路，以及使用CIBERSORT反卷积算法进行组织转录组免疫浸润水平外推和单细胞转录组数据校正。通过将高脂饮食与5Gyγ射线全身低剂量电离辐射相结合来构建动物模型。通过酶联免疫吸附试验验证了NETs释放的检测。
结果：分析揭示了辐射后和动脉粥样硬化两个数据集中的共有基因，提示免疫系统中性粒细胞可能是连接辐射和动脉粥样硬化的关键节点。NETs释放的中性粒细胞逝世亡能够影响动脉粥样硬化的发展。动物实验表明,低剂量辐射后中性粒细胞数量减少(P<0.05),NETs浓度降低,HF组NETs浓度显著升高(P<0.05)。与对照组相比，高脂饲料组血管内皮斑块明显增多，低剂量辐射组血管内皮斑块明显减少。
结论：长期低剂量电离辐射照射刺激嗜中性粒细胞并抑制其产生NETs，导致动脉粥样硬化的抑制。
