Biogen Idec Inc, 14 Cambridge Center, Cambridge, MA 02142, USA.
Mol Cell Neurosci. 2011 Apr;46(4):752-61. doi: 10.1016/j.mcn.2011.02.008. Epub 2011 Feb 23.
OMgp is selectively expressed in CNS by oligodendrocyte. However, its potential role(s) in oligodendrocyte development and myelination remain unclear. We show that OMgp null mice are hypomyelinated in their spinal cords, resulting in slower ascending and descending conduction velocities compared to wild-type mice. Consistent with the hypomyelination, in the MOG induced EAE model, OMgp null mice show a more severe EAE clinical disease and slower nerve conduction velocity compared to WT animals. The contribution of OMgp to oligodendrocyte differentiation and myelination was verified using cultured oligodendrocytes from null mice. Oligodendrocytes isolated from OMgp null mice show a significant decrease in the number of MBP(+) cells and in myelination compared to wild-type mice. The dramatic effects of the OMgp KO in oligodendrocyte maturation in vivo and in vitro reveal a new and important function for OMgp in regulating CNS myelination.
OMgp 由少突胶质细胞特异性表达于中枢神经系统。然而，其在少突胶质细胞发育和髓鞘形成中的潜在作用尚不清楚。我们发现，OMgp 基因敲除小鼠的脊髓发生低髓鞘化，与野生型小鼠相比，上行和下行传导速度较慢。与低髓鞘化一致的是，在髓鞘碱性蛋白诱导的实验性自身免疫性脑脊髓炎模型中，与 WT 动物相比，OMgp 基因敲除小鼠表现出更严重的 EAE 临床疾病和更慢的神经传导速度。利用从基因敲除小鼠中分离的少突胶质细胞培养物验证了 OMgp 对少突胶质细胞分化和髓鞘形成的作用。与野生型小鼠相比，从 OMgp 基因敲除小鼠中分离的少突胶质细胞中，MBP(+)细胞数量和髓鞘形成明显减少。OMgp KO 在体内和体外对少突胶质细胞成熟的显著影响揭示了 OMgp 在调节中枢神经系统髓鞘形成中的一个新的和重要的功能。
