Chromatin remodeling and epigenetic regulation of oligodendrocyte myelination and myelin repair.
Chromatin remodeling and epigenetic regulation of oligodendrocyte myelination and myelin repair.
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DOI：
10.1016/j.mcn.2017.11.010
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发表时间：
2018-03
期刊：
影响因子：
--
通讯作者：
Lu QR
中科院分区：
文献类型：
--
作者：
Koreman E;Sun X;Lu QR
少突胶质细胞对于脊椎动物中枢神经系统的发育、功能和健康是必不可少的。这些细胞维持轴突髓鞘形成以确保动作电位的跳跃式传播。少突胶质细胞从神经前体细胞发育而来，在一个涉及少突胶质细胞前体特化、增殖和分化的逐步过程中。谱系进展需要协调转录和表观遗传回路来介导少突胶质细胞发育的阶段特异性复杂性。表观遗传机制涉及DNA甲基化、组蛋白修饰、ATP依赖性染色质重塑和非编码RNA调节，其通过调节基因调节染色质状态，所述调节基因必须被表达或抑制以建立少突胶质细胞身份和谱系进展。在这篇综述中，我们将重点关注与组蛋白修饰酶、染色质重塑和调节少突胶质细胞谱系进展的非编码RNA相关的表观遗传编程，并讨论如何利用这些机制诱导髓鞘修复以治疗脱髓鞘疾病，如多发性硬化症。
Oligodendrocytes are essential for the development, function, and health of the vertebrate central nervous system. These cells maintain axon myelination to ensure saltatory propagation of action potentials. Oligodendrocyte develops from neural progenitor cells, in a step-wise process that involves oligodendrocyte precursor specification, proliferation, and differentiation. The lineage progression requires coordination of transcriptional and epigenetic circuits to mediate the stage-specific intricacies of oligodendrocyte development. Epigenetic mechanisms involve DNA methylation, histone modifications, ATP-dependent chromatin remodeling, and non-coding RNA modulation that regulate the chromatin state over regulatory genes, which must be expressed or repressed to establish oligodendrocyte identity and lineage progression. In this review, we will focus on epigenetic programming associated with histone modification enzymes, chromatin remodeling, and non-coding RNAs that regulate oligodendrocyte lineage progression, and discuss how these mechanisms might be harnessed to induce myelin repair for treatment of demyelinating diseases such as multiple sclerosis.
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