Department of Genetics, Cell Biology, and Anatomy, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
Division of Radioprotectants, Department of Pharmacology and Molecular Therapeutics, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
BMC Genomics. 2023 May 22;24(1):274. doi: 10.1186/s12864-023-09385-3.
The risk of exposure of the general public or military personnel to high levels of ionizing radiation from nuclear weapons or radiological accidents is a dire national security matter. The development of advanced molecular biodosimetry methods, those that measure biological response, such as transcriptomics, to screen large populations of radiation-exposed victims is key to improving survival outcomes during radiological mass casualty scenarios. In this study, nonhuman primates were exposed to either 12.0 Gy cobalt-60 gamma (total-body irradiation, TBI) or X-ray (partial-body irradiation, PBI) 24 h after administration of a potential radiation medical countermeasure, gamma-tocotrienol (GT3). Changes in the jejunal transcriptomic profiles in GT3-treated and irradiated animals were compared to healthy controls to assess the extent of radiation damage. No major effect of GT3 on radiation-induced transcriptome at this radiation dose was identified. About 80% of the pathways with a known activation or repression state were commonly observed between both exposures. Several common pathways activated due to irradiation include FAK signaling, CREB signaling in the neurons, phagosome formation, and G-protein coupled signaling pathway. Sex-specific differences associated with excessive mortality among irradiated females were identified in this study, including Estrogen receptor signaling. Differential pathway activation was also identified across PBI and TBI, pointing towards altered molecular response for different degrees of bone marrow sparing and radiation doses. This study provides insight into radiation-induced changes in jejunal transcriptional profiles, supporting the investigation for the identification of biomarkers for radiation injury and countermeasure efficacy.
公众或军事人员暴露于核武器或放射性事故产生的高水平电离辐射的风险是一个严峻的国家安全问题。开发先进的分子生物剂量测定方法,即测量生物反应(如转录组学)的方法,以筛选大量辐射暴露受害者,是改善放射性大规模伤亡情况下生存结果的关键。在这项研究中,非人类灵长类动物在接受潜在的辐射医疗对策γ-生育三烯酚(GT3)治疗 24 小时后,接受了 12.0 Gy 钴-60γ(全身照射,TBI)或 X 射线(部分身体照射,PBI)照射。将 GT3 处理和辐照动物的空肠转录组谱变化与健康对照进行比较,以评估辐射损伤的程度。在这个辐射剂量下,GT3 对辐射诱导的转录组没有明显的影响。大约 80%具有已知激活或抑制状态的途径在两种暴露之间是共同观察到的。由于照射而激活的几个常见途径包括 FAK 信号、神经元中的 CREB 信号、吞噬体形成和 G 蛋白偶联信号通路。本研究在雌性辐射过量死亡率方面确定了与雌性有关的性别特异性差异,包括雌激素受体信号。在 PBI 和 TBI 之间也发现了差异途径激活,这表明不同程度的骨髓保护和辐射剂量下的分子反应发生了改变。这项研究提供了对空肠转录谱中辐射诱导变化的深入了解,支持了对辐射损伤和对策功效的生物标志物的鉴定。