DNA methylation in Schwann cells and in oligodendrocytes
DNA methylation in Schwann cells and in oligodendrocytes
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DOI：
10.1002/glia.23784
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发表时间：
2020-01-20
期刊：
影响因子：
6.2
通讯作者：
Moyon, Sarah
中科院分区：
文献类型：
--
作者：
Arthur-Farraj, Peter;Moyon, Sarah
DNA甲基化是许多表观遗传标记之一，它在多步循环中直接修饰碱基残基，通常是胞嘧啶。它与几种细胞类型中基因表达和选择性剪接的调节有关，包括在细胞谱系特化和分化过程中。在衰老过程中也观察到DNA甲基化的变化，并且在几种神经系统疾病中已经报道了异常的甲基化模式。我们在这里审查的作用，雪旺细胞和少突胶质细胞，髓鞘形成的神经胶质细胞的外周和中枢神经系统，分别在DNA甲基化。我们首先讨论了甲基化和去甲基化是如何调节髓鞘形成细胞在发育和修复过程中的分化的。然后，我们提到疾病和癌症中的DNA甲基化失调如何通过直接影响髓鞘细胞的增殖和分化能力来解释其发病机制。
DNA methylation is one of many epigenetic marks, which directly modifies base residues, usually cytosines, in a multiple-step cycle. It has been linked to the regulation of gene expression and alternative splicing in several cell types, including during cell lineage specification and differentiation processes. DNA methylation changes have also been observed during aging, and aberrant methylation patterns have been reported in several neurological diseases. We here review the role of DNA methylation in Schwann cells and oligodendrocytes, the myelin-forming glia of the peripheral and central nervous systems, respectively. We first address how methylation and demethylation are regulating myelinating cells' differentiation during development and repair. We then mention how DNA methylation dysregulation in diseases and cancers could explain their pathogenesis by directly influencing myelinating cells' proliferation and differentiation capacities.