Oligodendrocytes engineered with migratory proteins as effective graft source for cell transplantation in multiple sclerosis.

Ike de la Pena, Mibel Pabon, Sandra Acosta, Paul R Sanberg, Naoki Tajiri, Yuji Kaneko, Cesar V Borlongan
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引用次数: 9

Abstract

Multiple sclerosis (MS) is characterized by widespread immunomodulatory demyelination of the CNS resulting in nerve cell dysfunction. Accordingly, treatment strategies have been centered on immunodulation and remyelination, with the former primarily focused on reducing the pathology rather than enhancing myelin repair which the latter targets. While conceding to the emerging view of heterogeneity in the pathology of MS, which precludes variations in degree of immune response (i.e., inflammation) and demyelination, the concept of enhancing myelin repair is appealing since it is likely to provide both disease-reducing and disease-inhibiting therapeutic approach to MS. In this regard, we and several others, have proposed that cell replacement therapy is an effective strategy to repair the myelin in MS. Here, we hypothesize that transplantation of mouse bone marrow-derived oligodendrocytes (BMDOs) and BMDOs transfected with Ephrin proteins (BMDO+Ephrin), which are known to enhance cell and axonal migratory capacity, may produce therapeutic benefits in animal models of MS.

迁移蛋白工程少突胶质细胞作为多发性硬化症细胞移植的有效移植物来源。
多发性硬化症(MS)的特点是中枢神经系统广泛的免疫调节性脱髓鞘,导致神经细胞功能障碍。因此,治疗策略集中于免疫调节和髓鞘再生,前者主要侧重于减少病理,而不是增强髓鞘修复,后者的目标。虽然承认多发性硬化症病理异质性的新观点,它排除了免疫反应(即炎症)和脱髓鞘程度的变化,但增强髓磷脂修复的概念很有吸引力,因为它可能为多发性硬化症提供减少疾病和抑制疾病的治疗方法。在这方面,我们和其他几个人提出细胞替代疗法是修复多发性硬化症髓磷脂的有效策略。我们假设移植小鼠骨髓源性少突胶质细胞(BMDO)和转染Ephrin蛋白(BMDO+Ephrin)的BMDO可以增强细胞和轴突的迁移能力,可能对MS动物模型产生治疗效果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cell medicine
Cell medicine MEDICINE, RESEARCH & EXPERIMENTAL-
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