视神经一旦受损很难恢复。日本大阪大学和东北大学的一个联合研究小组日前宣布，他们通过抑制神经细胞内某种酶的作用，令实验鼠受损的视神经得以修复。
大阪大学教授山下俊英和东北大学教授高井俊行率领的研究小组发现，在神经细胞中发挥作用的一种蛋白酪氨酸磷酸酶SHP会妨碍神经再生。于是，他们设法抑制SHP发挥作用，结果显示，促进神经生长蛋白质的功能可以随之提高1.4倍。对视神经完全受损小鼠进行的实验进一步证实，通过向小鼠眼球中注入SHP抑制剂，小鼠的视神经在两周后可以得到修复。
山下俊英说，这一成果还可应用于中枢神经系统的再生，并将有助于开发神经系统修复新药。
相关论文已刊登在新一期《欧洲分子生物学组织杂志》（The EMBO Journal）上。（生物谷Bioon.com）
生物谷推荐原文出处：
The EMBO Journal doi:10.1038/emboj.2011.55
Myelin suppresses axon regeneration by PIR-B/SHP-mediated inhibition of Trk activity
Yuki Fujita, Shota Endo, Toshiyuki Takai and Toshihide Yamashita
Abstract
Paired immunoglobulin-like receptor B (PIR-B) partially mediates the regeneration-inhibiting effects of the myelin-derived protein Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte-myelin glycoprotein (OMgp). In this study, we report that inhibition of the PIR-B signaling cascades in neurons enhances axon regeneration in the central nervous system (CNS). Binding of MAG to PIR-B led to the association of PIR-B with tropomyosin receptor kinase (Trk) neurotrophin receptors. Src homology 2-containing protein tyrosine phosphatase (SHP)-1 and SHP-2, which were recruited to PIR-B upon MAG binding, functioned as Trk tyrosine phosphatases. Further, SHP-1 and SHP-2 inhibition reduced MAG-induced dephosphorylation of Trk receptors and abolished the inhibitory effect of MAG on neurite growth. Thus, PIR-B associated with Trk to downregulate basal and neurotrophin-regulated Trk activity through SHP-1/2 in neurons. Moreover, in vivo transfection of small interfering RNA (siRNA) for SHP-1 or SHP-2 induced axonal regeneration after optic nerve injury in mice. Our results thus identify a new molecular target to enhance regeneration of the injured CNS.
