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THE JOURNAL OF BIOLOGICAL CHEMISTRY: The Biochemical Behavior of LeadL I. Influence of Calcium, Phosphorus, and Vitamin D on Lead in Blood and Bone

Oligodendrocytes are the critical cell types giving rise to the myelin nerve sheath enabling efficient nerve transmission in the central nervous system (CNS). Oligodendrocyte precursor cells differentiate into mature oligodendrocytes and are maintained throughout life. Deficits in the generation, proliferation, or differentiation of these cells or their maintenance have been linked to neurological disorders ranging from developmental disorders to neurodegenerative diseases and limit repair after CNS injury. Understanding the regulation of these processes is critical for achieving proper myelination during development, preventing disease, or recovering from injury. Many of the key factors underlying these processes are epigenetic regulators that enable the fine tuning or reprogramming of gene expression during development and regeneration in response to changes in the local microenvironment. These include chromatin remodelers, histone-modifying enzymes, covalent modifiers of DNA methylation, and RNA modification–mediated mechanisms. In this review, we will discuss the key components in each of these classes which are responsible for generating and maintaining oligodendrocyte myelination as well as potential targeted approaches to stimulate the regenerative program in developmental disorders and neurodegenerative diseases.

Epigenetic regulation of oligodendrocyte myelination in developmental disorders and neurodegenerative diseases

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.

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DNA methylation in Schwann cells and in oligodendrocytes

DNA methylation is critical for oligodendrocyte development. The role of the converse process, DNA demethylation regulated by Ten-Eleven-Translocation (TET) dioxygenases, in oligodendrocyte homeostasis, myelination and remyelination however remains elusive. Here, we identify a genome-wide and locus-specific DNA hydroxymethylation landscape shift during oligodendrocyte progenitor cell (OPC) differentiation. Tet1 ablation results in defects in oligodendrocyte development and myelination in the developing brain, while impairing remyelination after demyelination in adult brains. Transcriptomic and DNA hydroxymethylation analyses reveal a TET1-regulated epigenetic program for oligodendrocyte differentiation and identify a set of target genes associated with Ca2+ homeostasis. Tet1-deficient OPCs exhibited reduced [Ca2+] oscillations, while activation of calcium channels partially restores the differentiation defect of Tet1-deficient OPCs. Moreover, dysregulated oligodendrocyte homeostasis caused by Tet1-deficiency impairs action potential propagation and synaptic transmission. Thus, our results suggest that stage-specific TET1-mediated epigenetic programming of oligodendrocyte homeostasis is required for proper myelination and repair as well as neuronal physiology in cell-autonomous and non-cell-autonomous mechanisms, respectively.

/pdf/tet1-mediated-oligodendrocyte-homeostasis-regulates-23wsbizujf.pdf

TET1-mediated Oligodendrocyte Homeostasis Regulates Myelination and Synaptic Functions

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TET1-mediated Oligodendrocyte Homeostasis Regulates Myelination and Synaptic Functions