Abstract:
:Thyroid hormone plays an important role in central nervous system (CNS) development, including the myelination of variable axonal calibers. It is well-established that thyroid hormone is required for the terminal differentiation of oligodendrocyte precursor cells (OPCs) into myelinating oligodendrocytes by inducing rapid cell-cycle arrest and constant transcription of pro-differentiation genes. This is well supported by the hypomyelinating phenotypes exhibited by patients with congenital hypothyroidism, cretinism. During development, myelinating oligodendrocytes only appear after the formation of neural circuits, indicating that the timing of oligodendrocyte differentiation is important. Since fetal and post-natal serum thyroid hormone levels peak at the stage of active myelination, it is suspected that the timing of oligodendrocyte development is finely controlled by thyroid hormone. The essential machinery for thyroid hormone signaling such as deiodinase activity (utilized by cells to auto-regulate the level of thyroid hormone), and nuclear thyroid hormone receptors (for gene transcription) are expressed on oligodendrocytes. In this review, we discuss the known and potential thyroid hormone signaling pathways that may regulate oligodendrocyte development and CNS myelination. Moreover, we evaluate the potential of targeting thyroid hormone signaling for white matter injury or disease.
journal_name
Mol Neurobioljournal_title
Molecular neurobiologyauthors
Lee JY,Petratos Sdoi
10.1007/s12035-016-0013-1subject
Has Abstractpub_date
2016-11-01 00:00:00pages
6568-6583issue
9eissn
0893-7648issn
1559-1182pii
10.1007/s12035-016-0013-1journal_volume
53pub_type
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