視神經(jīng)一旦受損很難恢復(fù),。日本大阪大學(xué)和東北大學(xué)的一個(gè)聯(lián)合研究小組日前宣布,，他們通過(guò)抑制神經(jīng)細(xì)胞內(nèi)某種酶的作用,，令實(shí)驗(yàn)鼠受損的視神經(jīng)得以修復(fù)。
大阪大學(xué)教授山下俊英和東北大學(xué)教授高井俊行率領(lǐng)的研究小組發(fā)現(xiàn),，在神經(jīng)細(xì)胞中發(fā)揮作用的一種蛋白酪氨酸磷酸酶SHP會(huì)妨礙神經(jīng)再生,。于是，他們?cè)O(shè)法抑制SHP發(fā)揮作用,，結(jié)果顯示,，促進(jìn)神經(jīng)生長(zhǎng)蛋白質(zhì)的功能可以隨之提高1.4倍。對(duì)視神經(jīng)完全受損小鼠進(jìn)行的實(shí)驗(yàn)進(jìn)一步證實(shí),，通過(guò)向小鼠眼球中注入SHP抑制劑,，小鼠的視神經(jīng)在兩周后可以得到修復(fù)。
山下俊英說(shuō),，這一成果還可應(yīng)用于中樞神經(jīng)系統(tǒng)的再生,，并將有助于開(kāi)發(fā)神經(jīng)系統(tǒng)修復(fù)新藥。
相關(guān)論文已刊登在新一期《歐洲分子生物學(xué)組織雜志》（The EMBO Journal）上,。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
