Lorenzetto Erika, Panteri Roger, Marino Ramona, Keller Flavio, Buffelli Mario
Dipartimento di Scienze Neurologiche e della Visione, Università di Verona, Strada Le Grazie n.8, 37134 Verona, Italy.
Eur J Neurosci. 2008 Jan;27(1):12-9. doi: 10.1111/j.1460-9568.2007.05978.x. Epub 2007 Dec 17.
Reelin, an extracellular matrix protein, plays an important role in the regulation of neuronal migration and cortical lamination in the developing brain. Little is known, however, about the role of this protein in axonal regeneration. We have previously shown that Reelin is secreted by Schwann cells in the peripheral nerve compartment during postnatal development and that it is up-regulated following nerve injury in adult mice. In this work, we generated mice deficient in Reelin (reeler) that express yellow fluorescent protein (YFP) in a subset of neurons and examined the axonal regeneration following nerve crush. We found that axonal regeneration was significantly altered compared with wild-type mice. By contrast, retrograde tracing with Fluorogold dye after sciatic nerve crush was unaffected in these mutants, being comparable with normal axonal transport observed in wild-type. These results indicate that the absence of Reelin impairs axonal regeneration following injury and support a role for this protein in the process of peripheral nerve regeneration.
Reelin是一种细胞外基质蛋白，在发育中的大脑中对神经元迁移和皮质分层的调节起着重要作用。然而，关于这种蛋白在轴突再生中的作用却知之甚少。我们之前已经表明，Reelin在出生后发育期间由周围神经节段中的雪旺细胞分泌，并且在成年小鼠神经损伤后会上调。在这项研究中，我们构建了Reelin基因缺失（reeler）且在一部分神经元中表达黄色荧光蛋白（YFP）的小鼠，并检查了神经挤压后的轴突再生情况。我们发现，与野生型小鼠相比，轴突再生发生了显著改变。相比之下，坐骨神经挤压后用荧光金染料进行的逆行追踪在这些突变体中未受影响，与在野生型中观察到的正常轴突运输相当。这些结果表明，Reelin的缺失会损害损伤后的轴突再生，并支持这种蛋白在周围神经再生过程中的作用。
