Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana.
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana.
Radiat Res. 2019 May;191(5):383-397. doi: 10.1667/RR15130.1. Epub 2019 Mar 22.
We have previously shown significant pathology in the heart and kidney of murine hematopoietic-acute radiation syndrome (H-ARS) survivors of 8.7-9.0 Gy total-body irradiation (TBI). The goal of this study was to determine temporal relationships in the development of vasculopathy and the progression of renal and cardiovascular delayed effects of acute radiation exposure (DEARE) at TBI doses less than 9 Gy and to elucidate the potential roles of senescence, inflammation and oxidative stress. Our results show significant loss of endothelial cells in coronary arteries by 4 months post-TBI (8.53 or 8.72 Gy of gamma radiation). This loss precedes renal dysfunction and interstitial fibrosis and progresses to abnormalities in the arterial media and adventitia and loss of coronary arterioles. Major differences in radiation-induced pathobiology exist between the heart and kidney in terms of vasculopathy progression and also in indices of inflammation, senescence and oxidative imbalance. The results of this work suggest a need for different medical countermeasures for multiple targets in different organs and at various times after acute radiation injury to prevent the progression of DEARE.
我们之前已经在接受 8.7-9.0 Gy 全身照射(TBI)的造血性急性辐射综合征(H-ARS)小鼠的心脏和肾脏中发现了明显的病变。本研究的目的是确定血管病变的发展以及肾脏和心血管急性辐射暴露延迟效应(DEARE)在小于 9 Gy 的 TBI 剂量下的进展之间的时间关系,并阐明衰老、炎症和氧化应激的潜在作用。我们的结果显示,TBI 后 4 个月(γ射线 8.53 或 8.72 Gy),冠状动脉内皮细胞明显丢失。这种丢失先于肾功能障碍和间质纤维化,并进展为动脉中层和外膜的异常以及冠状动脉小动脉的丢失。在血管病变的进展以及炎症、衰老和氧化失衡的指标方面,心脏和肾脏之间的辐射诱导病理生物学存在显著差异。这项工作的结果表明,需要针对不同器官和急性辐射损伤后不同时间的多个靶标采取不同的医疗对策,以防止 DEARE 的进展。