Department of Biology, Institute of Cell Biology, ETH Zurich, ETH-Hönggerberg, HPM E39, Schafmattstrasse 18, CH-8093 Zürich, Switzerland.
Mol Neurobiol. 2011 Dec;44(3):303-12. doi: 10.1007/s12035-011-8198-9. Epub 2011 Aug 23.
Myelinated axons are a beautiful example of symbiotic interactions between two cell types: Myelinating glial cells organize axonal membranes and build their myelin sheaths to allow fast action potential conduction, while axons regulate myelination and enhance the survival of myelinating cells. Axonal demyelination, occurring in neurodegenerative diseases or after a nerve injury, results in severe motor and/or mental disabilities. Thus, understanding how the myelination process is induced, regulated, and maintained is crucial to develop new therapeutic strategies for regeneration in the nervous system. Epigenetic regulation has recently been recognized as a fundamental contributing player. In this review, we focus on the central mechanisms of gene regulation mediated by histone deacetylation and other key functions of histone deacetylases in Schwann cells and oligodendrocytes, the myelinating glia of the peripheral and central nervous systems.
少突胶质细胞将轴突膜组织化并构建髓鞘，以允许快速动作电位传导，而轴突调节髓鞘形成并增强少突胶质细胞的存活。脱髓鞘发生在神经退行性疾病或神经损伤后，导致严重的运动和/或精神残疾。因此，了解髓鞘形成过程是如何被诱导、调节和维持的，对于开发神经系统再生的新治疗策略至关重要。最近，人们认识到表观遗传调控是一个基本的促成因素。在这篇综述中，我们专注于由组蛋白去乙酰化介导的基因调控的中心机制，以及组蛋白去乙酰酶在周围和中枢神经系统的髓鞘形成胶质细胞——少突胶质细胞和寡突胶质细胞中的其他关键功能。
