Center for Musculoskeletal Disease Research and Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Little Rock, AR 72205, USA.
Department of Pharmaceutical Sciences, Division of Radiation Health, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Little Rock, AR 72205, USA.
Int J Mol Sci. 2021 Oct 28;22(21):11711. doi: 10.3390/ijms222111711.
Space is a high-stress environment. One major risk factor for the astronauts when they leave the Earth's magnetic field is exposure to ionizing radiation from galactic cosmic rays (GCR). Several adverse changes occur in mammalian anatomy and physiology in space, including bone loss. In this study, we assessed the effects of simplified GCR exposure on skeletal health in vivo. Three months following exposure to 0.5 Gy total body simulated GCR, blood, bone marrow and tissue were collected from 9 months old male mice. The key findings from our cell and tissue analysis are (1) GCR induced femoral trabecular bone loss in adult mice but had no effect on spinal trabecular bone. (2) GCR increased circulating osteoclast differentiation markers and osteoclast formation but did not alter new bone formation or osteoblast differentiation. (3) Steady-state levels of mitochondrial reactive oxygen species, mitochondrial and non-mitochondrial respiration were increased without any changes in mitochondrial mass in pre-osteoclasts after GCR exposure. (4) Alterations in substrate utilization following GCR exposure in pre-osteoclasts suggested a metabolic rewiring of mitochondria. Taken together, targeting radiation-mediated mitochondrial metabolic reprogramming of osteoclasts could be speculated as a viable therapeutic strategy for space travel induced bone loss.
太空是一个高压力的环境。当宇航员离开地球磁场时,一个主要的风险因素是暴露在来自银河宇宙射线(GCR)的电离辐射下。在太空中,哺乳动物的解剖结构和生理学发生了几种不良变化,包括骨质流失。在这项研究中,我们评估了简化 GCR 暴露对体内骨骼健康的影响。在接受 0.5Gy 全身模拟 GCR 照射 3 个月后,从 9 个月大的雄性小鼠中采集血液、骨髓和组织。我们的细胞和组织分析的主要发现是:(1)GCR 诱导成年小鼠股骨小梁骨丢失,但对脊柱小梁骨没有影响。(2)GCR 增加了循环破骨细胞分化标志物和破骨细胞形成,但不改变新骨形成或成骨细胞分化。(3)在 GCR 暴露后,破骨细胞前体细胞中线粒体活性氧、线粒体和非线粒体呼吸的稳态水平增加,但线粒体质量没有变化。(4)GCR 暴露后破骨细胞前体细胞中底物利用的改变表明线粒体的代谢重编程。总之,靶向辐射介导的破骨细胞线粒体代谢重编程可能被推测为太空旅行引起的骨质流失的可行治疗策略。