Journal
MOLECULAR NEUROBIOLOGY
Volume 53, Issue 9, Pages 6568-6583Publisher
SPRINGER
DOI: 10.1007/s12035-016-0013-1
Keywords
Thyroid hormone; Oligodendrocyte; Myelination; Thyroid hormone transport
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Funding
- Multiple Sclerosis Research Australia Postgraduate Scholarship
- Trish Multiple Sclerosis Research Foundation
- National Multiple Sclerosis Society Project [RG4398A1/1]
- International Progressive Multiple Sclerosis Alliance Challenge award [PA0065]
- Trish Multiple Sclerosis Research Foundation [15-022]
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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.
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