Muralidharan Sujatha, Sasi Sharath P, Zuriaga Maria A, Hirschi Karen K, Porada Christopher D, Coleman Matthew A, Walsh Kenneth X, Yan Xinhua, Goukassian David A
Whitaker Cardiovascular Institute, Boston University School of Medicine , Boston, MA , USA.
Cardiovascular Research Center, GeneSys Research Institute , Boston, MA , USA.
Front Oncol. 2015 Oct 14;5:231. doi: 10.3389/fonc.2015.00231. eCollection 2015.
Exposure of individuals to ionizing radiation (IR), as in the case of astronauts exploring space or radiotherapy cancer patients, increases their risk of developing secondary cancers and other health-related problems. Bone marrow (BM), the site in the body where hematopoietic stem cell (HSC) self-renewal and differentiation to mature blood cells occurs, is extremely sensitive to low-dose IR, including irradiation by high-charge and high-energy particles. Low-dose IR induces DNA damage and persistent oxidative stress in the BM hematopoietic cells. Inefficient DNA repair processes in HSC and early hematopoietic progenitors can lead to an accumulation of mutations whereas long-lasting oxidative stress can impair hematopoiesis itself, thereby causing long-term damage to hematopoietic cells in the BM niche. We report here that low-dose (1)H- and (56)Fe-IR significantly decreased the hematopoietic early and late multipotent progenitor (E- and L-MPP, respectively) cell numbers in mouse BM over a period of up to 10 months after exposure. Both (1)H- and (56)Fe-IR increased the expression of pluripotent stem cell markers Sox2, Nanog, and Oct4 in L-MPPs and 10 months post-IR exposure. We postulate that low doses of (1)H- and (56)Fe-IR may induce endogenous cellular reprogramming of BM hematopoietic progenitor cells to assume a more primitive pluripotent phenotype and that IR-induced oxidative DNA damage may lead to mutations in these BM progenitors. This could then be propagated to successive cell lineages. Persistent impairment of BM progenitor cell populations can disrupt hematopoietic homeostasis and lead to hematologic disorders, and these findings warrant further mechanistic studies into the effects of low-dose IR on the functional capacity of BM-derived hematopoietic cells including their self-renewal and pluripotency.
个体暴露于电离辐射(IR)下,比如宇航员探索太空或癌症患者接受放射治疗时,会增加患继发性癌症和其他健康相关问题的风险。骨髓(BM)是体内造血干细胞(HSC)自我更新并分化为成熟血细胞的场所,对低剂量IR极为敏感,包括受到高电荷和高能粒子的照射。低剂量IR会在BM造血细胞中诱导DNA损伤和持续的氧化应激。HSC和早期造血祖细胞中低效的DNA修复过程会导致突变积累,而长期的氧化应激会损害造血作用本身,从而对BM微环境中的造血细胞造成长期损伤。我们在此报告,低剂量的氢-1和铁-56 IR在暴露后长达10个月的时间里,显著降低了小鼠BM中造血早期和晚期多能祖细胞(分别为E-MPP和L-MPP)的数量。氢-1和铁-56 IR在L-MPP中以及IR暴露后10个月均增加了多能干细胞标志物Sox2、Nanog和Oct4的表达。我们推测,低剂量的氢-1和铁-56 IR可能诱导BM造血祖细胞发生内源性细胞重编程,使其呈现出更原始的多能表型,并且IR诱导的氧化性DNA损伤可能导致这些BM祖细胞发生突变。这进而可能传播至后续的细胞谱系。BM祖细胞群体的持续受损会破坏造血稳态并导致血液学紊乱,这些发现值得对低剂量IR对BM来源的造血细胞功能能力(包括其自我更新和多能性)的影响进行进一步的机制研究。