Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Cell Mol Life Sci. 2014 Mar;71(6):1055-66. doi: 10.1007/s00018-013-1488-9. Epub 2013 Oct 17.
It is now relatively well accepted that the cerebrovascular system does not merely provide inert pipes for blood delivery to the brain. Cerebral endothelial cells may compose an embedded bunker of trophic factors that contribute to brain homeostasis and function. Recent findings suggest that soluble factors from cerebral endothelial cells nourish neighboring cells, such as neurons and astrocytes. Although data are strongest in supporting mechanisms of endothelial-neuron and/or endothelial-astrocyte trophic coupling, it is likely that similar interactions also exist between cerebral endothelial cells and oligodendrocyte lineage cells. In this mini-review, we summarize current advances in the field of endothelial-oligodendrocyte trophic coupling. These endothelial-oligodendrocyte interactions may comprise the oligovascular niche to maintain their cellular functions and sustain ongoing angiogenesis/oligodendrogenesis. Importantly, it should be noted that the cell-cell interactions are not static-the trophic coupling is disturbed under acute phase after brain injury, but would be recovered in the chronic phase to promote brain remodeling and repair. Oligodendrocyte lineage cells play critical roles in white matter function, and under pathological conditions, oligodendrocyte dysfunction lead to white matter damage. Therefore, a deeper understanding of the mechanisms of endothelial-oligodendrocyte trophic coupling may lead to new therapeutic approaches for white matter-related diseases, such as stroke or vascular dementia.
现在人们已经比较接受这样一种观点,即脑血管系统不仅仅是为大脑供血的惰性管道。脑内皮细胞可能构成了一个嵌入式的营养因子碉堡,有助于大脑的内稳定和功能。最近的发现表明,脑内皮细胞产生的可溶性因子为邻近的细胞,如神经元和星形胶质细胞提供营养。虽然数据最有力地支持内皮-神经元和/或内皮-星形胶质细胞营养偶联的机制,但内皮细胞与少突胶质细胞谱系细胞之间也可能存在类似的相互作用。在这篇迷你综述中,我们总结了内皮-少突胶质细胞营养偶联领域的最新进展。这些内皮-少突胶质细胞的相互作用可能构成了少突胶质细胞的血管龛,以维持其细胞功能,并维持持续的血管生成/少突胶质细胞发生。重要的是,应该注意到细胞-细胞相互作用不是静态的——在脑损伤后的急性期,营养偶联会受到干扰,但在慢性期会恢复,以促进大脑重塑和修复。少突胶质细胞谱系细胞在白质功能中起着关键作用,在病理条件下,少突胶质细胞功能障碍会导致白质损伤。因此,深入了解内皮-少突胶质细胞营养偶联的机制可能为与白质相关的疾病,如中风或血管性痴呆,提供新的治疗方法。