Department of Neurobiology, Stanford University, Fairchild Building D205, 299 Campus Drive West, Stanford, CA 94305, United States.
Curr Opin Neurobiol. 2013 Dec;23(6):914-20. doi: 10.1016/j.conb.2013.06.005. Epub 2013 Jul 3.
Oligodendrocytes (OLs) are the myelinating glia of the central nervous system. Myelin is essential for the rapid propagation of action potentials as well as for metabolic support of axons, and its loss in demyelinating diseases like multiple sclerosis has profound pathological consequences. The many steps in the development of OLs - from the specification of oligodendrocyte precursor cells (OPCs) during embryonic development to their differentiation into OLs that myelinate axons - are under tight regulation. Here we discuss recent advances in understanding how these steps of OL development are controlled intrinsically by transcription factors and chromatin remodeling and extrinsically by signaling molecules and neuronal activity. We also discuss how knowledge of these pathways is now allowing us to take steps toward generating patient-specific OPCs for disease modeling and myelin repair.
少突胶质细胞（OLs）是中枢神经系统的髓鞘形成胶质细胞。髓鞘对于动作电位的快速传播以及轴突的代谢支持至关重要，而脱髓鞘疾病（如多发性硬化症）中髓鞘的丢失会产生深远的病理后果。OLs 的许多发育步骤——从胚胎发育过程中少突胶质前体细胞（OPCs）的特化到分化为髓鞘形成轴突的 OLs——都受到严格的调控。在这里，我们讨论了最近在理解这些 OL 发育步骤如何通过转录因子和染色质重塑内在控制以及通过信号分子和神经元活动外在控制方面的进展。我们还讨论了这些途径的知识如何使我们能够朝着为疾病建模和髓鞘修复生成患者特异性 OPCs 的方向迈出一步。
