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Advancing Stem Cell Therapy for Repair of Damaged LungMicrovasculature in Amyotrophic Lateral Sclerosis

机译：推进干细胞疗法治疗受损肺部修复肌萎缩侧面硬化症中的微血管

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Amyotrophic lateral sclerosis (ALS) is a fatal disease of motor neurondegeneration in the brain and spinal cord. Progressive paralysis ofthe diaphragm and other respiratory muscles leading to respiratorydysfunction and failure is the most common cause of death in ALSpatients. Respiratory impairment has also been shown in animal modelsof ALS. Vascular pathology is another recently recognized hallmark ofALS pathogenesis. Central nervous system (CNS) capillary damage is ashared disease element in ALS rodent models and ALS patients.Microvascular impairment outside of the CNS, such as in the lungs, mayoccur in ALS, triggering lung damage and affecting breathing function.Stem cell therapy is a promising treatment for ALS. However, thistherapeutic strategy has primarily targeted rescue of degeneratedmotor neurons. We showed functional benefits from intravenous deliveryof human bone marrow (hBM) stem cells on restoration of capillaryintegrity in the CNS of an superoxide dismutase 1 (SOD1) mouse modelof ALS. Due to the widespread distribution of transplanted cells viathis route, administered cells may enter the lungs and effectivelyrestore microvasculature in this respiratory organ. Here, we providedpreliminary evidence of the potential role of microvasculaturedysfunction in prompting lung damage and treatment approaches forrepair of respiratory function in ALS. Our initial studies showedproof-of-principle that microvascular damage in ALS mice results inlung petechiae at the late stage of disease and that systemictransplantation of mainly hBM-derived endothelial progenitor cellsshows potential to promote lung restoration via re-establishedvascular integrity. Our new understanding of previously underexploredlung competence in this disease may facilitate therapy targetingrestoration of respiratory function in ALS.
机译：肌营养的外侧硬化症（ALS）是运动神经元的致命疾病脑和脊髓的变性。渐进瘫痪隔膜和其他导致呼吸的呼吸肌肉功能障碍和失败是ALS中最常见的死因耐心。呼吸障碍也已在动物模型中显示als。血管病理学是另一个最近认可的标志ALS发病机制。中枢神经系统（CNS）毛细管损坏是一个ALS啮齿动物模型和ALS患者的共同疾病元素。在CNS之外的微血管损伤，例如在肺部，可能是发生在ALS，触发肺部损伤并影响呼吸功能。干细胞疗法是ALS的有希望的治疗方法。但是，这是这样的治疗策略主要有针对性的拯救运动神经元。我们展示了静脉内交付的功能效益人骨髓（HBM）干细胞毛细血管恢复超氧化物歧化酶1（SOD1）小鼠模型的CNS中的完整性als。由于通过普遍的移植细胞的普及分布该途径，施用细胞可以有效地进入肺部恢复在该呼吸道器官中的微血管。在这里，我们提供了微孔化潜在作用的初步证据促使肺部损伤和治疗方法的功能障碍修复ALS中的呼吸功能。我们的初步研究表明原则上的原则上，微血管损伤在als小鼠中导致在疾病后期的肺瘀点，系统性主要是HBM衍生的内皮祖细胞的移植通过重新建立，表明促进肺恢复的潜力血管完整性。我们对以前未引人注目的新了解这种疾病的肺功能可能有助于治疗靶向恢复血液中的呼吸功能。

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