a Scientific Research Department, Armed Forces Radiobiology Research Institute, Bethesda, Maryland.
b Biostatistics Consulting Center.
Radiat Res. 2018 Aug;190(2):164-175. doi: 10.1667/RR14993.1. Epub 2018 May 29.
Although bone marrow aplasia has been considered for the past decades as the major contributor of radiation-induced blood disorders, cytopenias alone are insufficient to explain differences in the prevalence of bleeding. In this study, the minipig was used as a novel preclinical model of hematopoietic acute radiation syndrome to assess if factors other than platelet counts correlated with bleeding and survival. We sought to determine whether radiation affected the insulin-like growth factor-1 (IGF-1) pathway, a growth hormone with cardiovascular and radioprotective features. Gottingen and Sinclair minipigs were exposed to ionizing radiation at hematopoietic doses. The smaller Gottingen minipig strain was more sensitive to radiation; differences in IGF-1 levels were minimal, suggesting that increased sensitivity could depend on weak response to the hormone. Radiation caused IGF-1 selective resistance by inhibiting the anti-inflammatory anti-oxidative stress IRS/PI3K/Akt but not the pro-inflammatory MAPK kinase pathway, shifting IGF-1 signaling towards a pro-oxidant, pro-inflammatory environment. Selective IGF-1 resistance associated with hemorrhages in the heart, poor prognosis, increase in C-reactive protein and NADPH oxidase 2, uncoupling of endothelial nitric oxide synthase, inhibition of nitric oxide (NO) synthesis and imbalance between the vasodilator NO and the vasoconstrictor endothelin-1 molecules. Selective IGF-1 resistance is a novel mechanism of radiation injury, associated with a vicious cycle amplifying reactive oxygen species-induced damage, inflammation and endothelial dysfunction. In the presence of thrombocytopenia, selective inhibition of IGF-1 cardioprotective function may contribute to the development of hemostatic disorders. This finding may be particularly relevant for individuals with low IGF-1 activity, such as the elderly or those with cardiometabolic dysfunctions.
虽然骨髓衰竭在过去几十年中被认为是辐射诱导血液疾病的主要原因,但单纯的细胞减少不足以解释出血患病率的差异。在这项研究中,小型猪被用作造血急性辐射综合征的新型临床前模型,以评估血小板计数以外的因素是否与出血和存活相关。我们试图确定辐射是否会影响胰岛素样生长因子-1(IGF-1)途径,这是一种具有心血管和辐射防护特性的生长激素。戈丁根和辛克莱尔小型猪接受了造血剂量的电离辐射。较小的戈丁根小型猪对辐射更敏感;IGF-1 水平的差异很小,这表明增加的敏感性可能取决于对激素的弱反应。辐射通过抑制抗炎抗氧化应激 IRS/PI3K/Akt 而不是促炎 MAPK 激酶途径来引起 IGF-1 选择性抵抗,从而将 IGF-1 信号转导转向促氧化剂、促炎环境。选择性 IGF-1 抵抗与心脏出血、预后不良、C 反应蛋白和 NADPH 氧化酶 2 增加、内皮一氧化氮合酶解偶联、一氧化氮(NO)合成抑制以及血管扩张剂 NO 和血管收缩剂内皮素-1 分子之间的失衡有关。选择性 IGF-1 抵抗是辐射损伤的一种新机制,与放大活性氧诱导损伤、炎症和内皮功能障碍的恶性循环有关。在血小板减少症的情况下,选择性抑制 IGF-1 的心脏保护功能可能有助于止血障碍的发展。这一发现对于 IGF-1 活性较低的个体(如老年人或存在心血管代谢功能障碍的个体)可能尤为相关。