Axonal plasticity and functional recovery after spinal cord injury in mice deficient in both glial fibrillary acidic protein and vimentin genes
Axonal plasticity and functional recovery after spinal cord injury in mice deficient in both glial fibrillary acidic protein and vimentin genes
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DOI：
10.1073/pnas.1533187100
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发表时间：
2003-07-22
影响因子：
11.1
通讯作者：
Ribotta, MGY
中科院分区：
文献类型：
--
作者：
Menet, V;Prieto, M;Ribotta, MGY
损伤的成年哺乳动物脊髓中轴突再生的缺乏导致永久性功能障碍。神经元轴突再生的能力很大程度上是由于星形胶质细胞瘢痕形成的不适宜生存的环境。我们产生了敲除胶质细胞酸性蛋白和波形蛋白的小鼠，这是星形胶质细胞细胞骨架的主要蛋白质，在反应性星形胶质细胞中上调。这些动物在脊髓半切后，表现出与脊髓上轴突的塑料发芽增加相关的星形胶质细胞反应性降低，包括导致功能恢复的电路重建。因此，在缺乏这两种蛋白质的情况下改善的解剖和功能恢复突出了反应性星形胶质细胞在成人CNS轴突再生失败中的关键作用，并可能导致脊髓损伤的新疗法。
The lack of axonal regeneration in the injured adult mammalian spinal cord leads to permanent functional disabilities. The inability of neurons to regenerate their axon is appreciably due to an inhospitable environment made of an astrocytic scar. We generated mice knock-out for glial fibrillary acidic protein and vimentin, the major proteins of the astrocyte cytoskeleton, which are up-regulated in reactive astrocytes. These animals, after a hemisection of the spinal cord, presented reduced astroglial reactivity associated with increased plastic sprouting of supraspinal axons, including the reconstruction of circuits leading to functional restoration. Therefore, improved anatomical and functional recovery in the absence of both proteins highlights the pivotal role of reactive astrocytes in axonal regenerative failure in adult CNS and could lead to new therapies of spinal cord lesions.