Regenerative therapy for spinal cord injury and their mechanism for reconstruction.

神经干细胞（NSCs）具有自我更新和分化为中枢神经系统（CNS）中发现的三种主要细胞类型的能力。近年来的研究表明，DNA甲基化和组蛋白修饰等表观遗传基因调控事件在调控NSC命运规范中起着重要作用。在此背景下，我们之前已经证明组蛋白去乙酰化酶抑制剂丙戊酸（VPA）可以增强NSCs的神经元分化。也许是因为这些NSC分化模式在正常胚胎发育过程中受到了精细的控制，因此受损成人中枢神经系统中受损神经网络的修复受到严重限制。本研究采用小鼠脊髓损伤模型，研究了VPA对NSC移植和分化控制的影响。

Neural stem cells(NSCs) possess the ability to self-renew and to differentiate into the three major cell types found in the central nervous system(CNS). Recent studies have shown that epigenetic gene regulation events such as DNA methylation and histone modification play important roles in regulating NSC fate specification. In this context, we have previously shown that the histone deacetylase inhibitor valproic acid(VPA) enhances neuronal differentiation of NSCs. Perhaps because these patterns of NSC differentiation are exquisitely controlled during normal embryonic development, restoration of damaged neural networks in the injured adult CNS is severely limited. Here, using a mouse model of spinal cord injury(SCI), we examined the effectiveness of NSC transplantation and differentiation control by VPA administration.