Combined intrinsic and extrinsic neuronal mechanisms facilitate bridging axonal regeneration one year after spinal cord injury.
Combined intrinsic and extrinsic neuronal mechanisms facilitate bridging axonal regeneration one year after spinal cord injury.
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DOI：
10.1016/j.neuron.2009.09.016
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发表时间：
2009-10-29
期刊：
影响因子：
16.2
通讯作者：
Tuszynski, Mark H.
中科院分区：
文献类型：
--
作者：
Kadoya, Ken;Tsukada, Shingo;Lu, Paul;Coppola, Giovanni;Geschwind, Dan;Filbin, Marie T.;Blesch, Armin;Tuszynski, Mark H.
尽管在促进急性脊髓损伤（SCI）后轴突再生方面取得了进展，但在慢性SCI后诱导桥接轴突再生仍然是一个艰巨的挑战。我们报告说，组合疗法管理6周，长达15个月，脊髓损伤后促进轴突再生进入和超越中颈病变部位。提供周围神经调节损伤，骨髓基质细胞移植和建立NT-3梯度，支持桥接再生。接收完整组合的部分组件的控件未能显示桥接。值得注意的是，延迟治疗的神经元内分子机制反映了急性损伤的机制，包括转录激活因子和再生相关基因的激活。总的来说，这些发现提供了证据，表明在前所未有的损伤后时间点再生是可以实现的。
Despite advances in promoting axonal regeneration after acute spinal cord injury (SCI), elicitation of bridging axon regeneration after chronic SCI remains a formidable challenge. We report that combinatorial therapies administered 6 weeks, and as long as 15 months, after SCI promote axonal regeneration into and beyond a mid-cervical lesion site. Provision of peripheral nerve conditioning lesions, grafts of marrow stromal cells and establishment of NT-3 gradients, supports bridging regeneration. Controls receiving partial components of the full combination fail to exhibit bridging. Notably, intraneuronal molecular mechanisms recruited by delayed therapies mirror those of acute injury, including activation of transcriptional activators and regeneration-associated genes. Collectively, these findings provide evidence that regeneration is achievable at unprecedented post-injury time points.
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